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DISEASES OF THE HEART

NOTE.

On the cover of this book is embossed an outline-
figure of the chest. If a piece of ordinary note-
paper be applied to this, and the point of a black-
lead pencil be drawn from side to side over the paper,
a " rubbing" will be obtained which will serve as a
" chest-chart/' and on which the situations of mur-
murs, the outlines of dulness, &c, can be indicated,
by coloured marks.

MANUAL

OF THE

PHYSICAL DIAGNOSIS

DISEASES OF THE HEART

INCLUDING TUE USE OF THE

SPHYGMO GRAPH AND CARDIOGRAPH

ARTHUR ERNEST SANSOM, M.D. Lond.

FELLOW OF THE ROYAL COLLEGE OF PHYSICIANS
ASSISTANT FH YSICI AN TO THE LONDON HOSPITAL
PHYSICIAN TU THE NORTH-EASTERN HOSPITAL FOR. CHILDREN
J-tmiEUT.Y PHYSICIAN TO THE ROYAL HOSPITAL FOR DISEASES OF THE CHEST, CITY ROAD
HONORARY FELLOW OF THE S1EDICAL SOCIETY, AND CORRESPONDING
MEMBER OF THE THERAPEUTICAL SOCIETY OF KF.W YORK

THIRD EDITION
LONDON

J. & A. CHURCHILL, NEW BURLINGTON STREET"

1881
[All rights reserved]

WELLCOME INSTITUTE
LIBRARY

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PBEFACE

THE THIKD EDITION.

The favourable reception accorded to former editions
Las convinced me that my little work supplied a want.
It was my aim to g'ive in a concise form the essentials
for the diagnosis of Diseases of the Heart according-
to the most modern teachings of pathology, tested,
confirmed, and extended, where possible, by personal
investigation. I wished that my book should be a
companion to the advanced student in the wards of
the hospital, and an aide-memoire to the practi-
tioner in his daily duties. Although the second
edition became rapidly exhausted, cardiac pathology
has made considerable progress since its publication ;
it has, therefore, been absolutely necessary to subject
the whole to thorough revision. To my regret, nearly
a twelvemonth has passed before I have been able to
complete this third edition.

The day has come when every educated practitioner
should be familiar with the use of the sphygmograpli
and cardiograph. The difficulties in the use of these
instruments, and especially the objection on account
of the time which their application occupies, are van-
ishing, owing to improvement in mechanism ; whilst
the value of the evidence which they afford is attested
by daily experience. As regards the systematic inves-

PHEI'ACE.

tigation of disease by such methods, much remains to
he done, hut, thank's to the labours of Drs. Galabin,
Mahomed, Balthazar- Foster, and others, as well as
to the introduction by Dr. Pond of an instrument
which can he employed readily and rapidly, data are
rapidly accumulating-. I have, therefore, endeavoured .
in this edition (though in the former I expressly
excluded the subject as premature) to describe the
methods of employment, and so far as observations
warrant, the indications of the sphygmograph and
cardiograph in cardiac diagnosis. The illustrations
of this portion of the work are for the most part
original, from tracings by myself or by my house-
physicians and clinical assistants under my own
direction. Among those who have rendered me efficient
aid I would especially mention Drs. S. D. Clipping-
dale and Needham, and Messrs. Major Greenwood,
Basil W. Walker, Burry, and Sweeting.

I indulge in a hope that I may be enabled to follow
up this little work with another on the Treatment of
Heart Disease, so arranged that the two volumes
shall constitute a systematic work.

SCHEMA.

I. — Symptomatology.

A. Symptoms referred to the Heart, (a.) Pain referred
directly to the Heart-region in cardiac disease is rare. Or-
ganic disease may progress without giving rise to Pain. The
special pain of Heart Disease is Angina Pectoris, characterized
by paroxysmal recurrence, great distress, coldness, arrest of
respiration. (b.) Palpitation: A frequent symptom in Heart
Disease, but common in dyspepsia and in emotional conditions,
(c.) Intermission : Common in Heart Disease, but may be
neurosal. {d.) Irregularity : Generally of grave import, but
may also be neurosal.

B. Symptoms referred to the Circulation, (a.) Pulsation:
Excluding emotional causes, suspect Hypertrophy of Heart,
and especially aortic regurgitation, (b.) Hcemorrhage : Common
in Heart Disease : Not of dangerous import as in Phthisis :
Note tendency thereto in mitral stenosis, (c. ) Cyanosis : Vide
Inspection, {d.) Dropsy : A late and dangerous symptom.

C. Symptoms referred to the Lungs. Note that these
symptoms are very frequent, {a.) Dyspnoea, aggravated by
exertion ; periodic or persistent, (b.) Cough.

D. Symptoms referred to the Brain, (a.) Languor and
poweiiessness. (&.) Vertigo and symptoms of disturbance of
cerebral circulation, (c.) Epdepsy. {d.) Chorea, (e.) Apo-
plexy. (/.) Paralysis.

Note. — In cases of cardiac hypertrophy co-existing with
renal disease, there may be intra-cranial hsernorrhage, some-
times difficult to distinguish from uraemia. In sudden cerebral
attacks in patients with valvular disease suspect Embolism.

E. Symptoms referred to the Alimentary Canal, (a.)
Dyspepsia, very common, (b.) Haemorrhoids.

F. Symptoms referred to the Throat, (a.) Pain referred to
the throat may be a variety of Angina. (b.) Aphonia
occasional in pericarditis, (c.) Hoarseness.

Vlll

SCHEMA.

0 symptoms referred to the Kidneys. (1.) Renal disease
may be induced by the Heart-affection. (2.) Renal disease
may induce hypertrophy of the Heart. (3. ) Renal and cardiac
disease may be the double effect of one cause.

Note.— In cases of Cardiac Disease, always examine the
urine, and especially record conditions of albuminuria.

II. — Etiology.

(a.) Rheumatism is the most frequent cause of valvular
Disease of the Heart. Rheumatic Fever is in a large number of
cases the starting-point, but in other cases the rheumatic
^ symptoms may be very slight and obscure, and sometimes the
rheumatic form of endocarditis may occur with no other
manifestation of rheumatism.

Note.— Examine the condition of the heart in the slight, as
well as in the severe forms of Rheumatism.

(&.) Scarlet .Fever is also a cause of valvular disease and of
pericarditis, probably because of the rheumatoid phenomena
associated with it. Measles also may be followed by heart-
disease, (c.) The other most common causes of Heart Disease
are muscular overstrain, alcoholism, syphilis, tubercidosis, the
puerperal state, poisoning by phosphorus, mal-nutrition,
disease contiguous to heart and pericardium, diseases of lung
induciug venous engorgement.

Note. — A satisfactory examination of any patient, what-
ever his .ailment, cannot be made unless the cardiac conditions
are observed and recorded.

Ill— Physical Examination — Inspection.

A. Hue of the surface, (a.) Blueness. (1.) Congenital
cyanosis indicates persistent foramen ovale, or imperfection of
inter-ventricular septum, usually combined with obstruction
of pulmonary artery. (2.) Intermittent cyanosis, common in
cardiac dyspnoea.

Note.— Chilling of finger-tips with blueness and coldness
common in Heart Disease.

(b.) Pallor. (1.) When associated with cedema, suspect co-
existence of renal disease. (2.) With exophthalmos, thyroid
enlargement and irritability of Heart, Graves' Disease.

SCHEMA.

(c) Tinge of Jaundice. (1.) In passive congestion of liver
in later stages of valvular disease. (2.) With arcus senilis in
Fatty Degeneration of Heart.

B. Cardiac Dyspnoea. (1.) Characterized by gasping air-
craving, aggravated by exertion — Orthopncea ; indicative of
valvular diseases, or cardiac degenerations.

(2.) Decubitus on right side, with expression of anxiety and
apprehension. Suspect Pericarditis.

0. (Edema: Commences in lower extremities, serous
cavities affected last : Usually depends on valvular disease
(especially mitral, or conjoined mitral disease and tricuspid
insufficiency).

Note. — Examine urine, and determine the question of co-
existence of renal and cardiac disease.

D. Pulsation, (a.) In veins of neck indicates tricuspid
insufficiency. (6.) In arteries : Locomotive pulse indicates
aortic regurgitation, (c.) Displacement outwards of visible
apex-beat indicates hypertrophy or dilatation of left ventricle.

Note. — Area of visible impulse may be apparently increased
at times in nervous palpitation.

(d.) Retraction of intercostal spaces coincidently with
systole indicates pericardial adhesions.

(c.) Pulsation of the liver indicates tricuspid regurgitation.

IV. — Physical Examination — Palpation.

A. Pulse, (a.) Rigid arteries, tortuous, with roughnesses
felt in their walls, associated with hard pulse, indicate
Atheroma.

(b. ) Slowness of pulse, with very weak impulse, may indi-
cate Fatty Degeneration.

(c.) Sudden variation of pulse with great acceleration on
movement may occur in Pericarditis.

(d.) Jerking, collapsing pulse in aortic regurgitation.

(e.) Feebleness of pulse, and (/.) Irregularity and inter-
mission, increased by effort, in mitral disease and cardiac
degeneration.

B. Apex-beat. Displaced. (1.) Upwards by pericardial
effusion. ■ (2.) Downwards and outwards in hypertrophy aud
dilatation of heart.

SCHI3MA.

ca,SlaFrCibr ?fSf °n fdt UUder falsc rihs t0 leftof ""iforui
ca. Wage indicates hypertrophy of right ventricle.

a»d dilatation of right chambers.

^ Visible pulsation of left auricle indicates mitral stenosis.

iNOTE that tins pulsation may be rendered evident by
vibrating levers.

Ji'JrCif CtrdiaC TaCtile Phenomena. (a.) Friction-fre-
mitus denoting Pericarditis, (b.) Thrill. (1.) Occurring with
systole over aortic valves denotes aortic stenosis or aneurism ;
over pulmonary valves, pulmonary stenosis; at apex, mitral
regurgitation. (2.) Occurring with diastole at base, denotes
aortic regurgitation, (3.) Occurring at apex just before, and
terminated by impulse, indicates mitral stenosis.

Note that decided presystolic thrill at apex is pathogno-
monic of mitral stenosis, and may occur without murmur"

V.— Physical Examination— Percussion .

A. Precordial area over-resonant or tympanitic— in em-
physema of lung, and in the very rare cases of pneumoperi-
cardium.

£. Precordial dulness extended, (a.) Upwards ; outline of
dull area being triangular or pyriform with apex at or above
third costo-sternal articulation. There is probably Efusion
nito pericardium. (6.) Laterally. The heart is enlarged by
hypertrophy or dilatation.

I. Lateral dulness extends left of normal area. (1.) Area
of dulness triangular, apex pointed, Hypertrophy of Left Ven-
tricle. (2.) Area of dulness rhomboidal, apex rounded, Dila-
tation of Left Ventricle.

Note.— Compare positiou of apex and outline of left ven-
tricle with evidences of force of apex-beat. If left side
enlargement with forcible heaving impulse and long first
sound, Hypertrophy. If enlargement with feeble impulse and
short first sound, Dilatation.

II. Lateral dulness extends right of normal area. There are
Hypertrophy and Dilatation of Right Auricle and Ventricle.

Note epigastric impulse and signs of tricuspid regurgitation,
if present.

SCHEMA.

VI.— Physical Examination— Auscultation.

Section I.— The normal heart-sounds are modified in degree.
A. At the base of the heart : —

(a.) The aortic second sound is intensified. There is Hyper-
trophy of the Left Ventricle.

(b.) The pulmonary second sound is intensified. There is
heightened tension in the pulmonic circulation.

Note. — A strong pulmonary, associated with a weak aortic
second sound, is presumptive evidence of mitral obstruction or
insufficiency.

B. At the apex of the heart : —

(a.) The first soimd is increased in duration. There is
Hypertrophy of Left Ventricle.

Note. — When there are signs of Hypertrophy of Left Ven-
tricle without other cardiac signs to account for it, suspect
Chronic Renal Disease.

(b.) The first sound is short, resembling the second sound.
There is feebleness, dilatation or degeneration of left ventricle.

Note. — Reduplication of heart-sounds occasionally occurs
in health ; when associated with fever or with grave debility,
indicates myocarditis or cardiac degeneration ; if reduplication
of second sound, suspect mitred stenosis.

Section II. Abnormal sounds are heard over the heart-
region.

A. Generally over the precordial area.

(a.) Friction sound indicates Acute Pericarditis — or Pericar-
dial roughening, the result of a remote pericarditis.

B. Localized in definite relation with the situations of the
valves.

(a.) First-sound murmur over site of aortic valves (anremia
excluded) indicates aortic obstruction.

Note.— The murmur may be localized or propagated in the
course of the great arteries.

(6.) Second-sound murmur over site of aortic valves indi-
cates aortic regurgitation.

Note. — This murmur may be localized, or propagated
downwards in the line of the sternum.

(c.) Double (first and second sound) murmur (a and b) de-
notes combined aortic obstruction and insufficiency.

xii

SCHEMA.

(cZ.) First-sound murmur over site of valves of pulmonary
artery denotes (anaemia and pressure upon trunk of pulmonary
artery excluded) obstruction of pulmonary artery.

Note.— Pulmonary obstruction is nearly always congenital.

(e.) First-sound murmur at base of ensiform cartilage indi.
cates tricuspid regurgitation.

Note. — This is most commonly found as secondary result of
mitral disease.

(/.) Before first-sound murmur- at base of ensiform cartilage
denotes tricuspid stenosis.

(g.) First-sound murmur heard over situation of right
ventricle may be due to myocarditis or anosmia with cardiac
debility.

Note. — These murmurs are not persistent.

(/i.) First-sound murmur localized in mitral area denotes
mitral regurgitation.

(i.) Before-first-sound murmur localized at apex, or just
internal thereto, denotes mitral stenosis— i.e., obstruction.

■v

PAET I.

THE ORDINARY METHODS OF PHYSICAL
DIAGNOSIS.

LECTURE I.

IN TRODDCTORY.

Symptomatology — Importance of subjective symptoms in
regard to treatment : of objective in diagnosis — Pain —
Angina pectoris — Cardiac symptoms — Disturbances of
circulation — Pulmonary symptoms — Cerebral phenomena —
Embolism— Gastric symptoms — Signs referred to the throat
— Renal symptoms — Etiology — Rheumatism — Other causes
of heart disease.

A few words on the threshold of the subject — advice
pertinent to investigation of disease in any form, but
yet I think rather particularly so to the class of diseases
which we shall presently examine. When a suffering-
patient comes to you for examination, do not permit a
diversity of purpose of intent to exist between your
mind and his. His chief object is to g-et relief from
his aches and pains ; yours, perhaps, is to find out —
by a process similar to that employed by botanists to
discover the name of a newly found flower — the name
of the disease which he suffers from. Remember that
your duty is not chiefly to find out what disease he is
the subject of, but what his sufferings are, what his
deviations from sound health. The plane of unhealth

INTRODUCTORY.

is divided into definite squares, which are called
Diseases, and the nomenclature of these is very im-
portant, because the mention of one of them displays
before the medical mind a large picture, and a moving
panorama of phenomena ; but your sole object is not
to find out into what particular square your patient's
aggregate of symptoms will fit. You must investigate
his ailments as well as his diseases if you would do
him good. I am very far from wishing to be a censor,
but I do think that in these days of great and increas-
ing precision in physical diagnosis, there is a real
clanger of students thinking too lightly of the uttered
complaints of patients. It has been said that one
objective sign is worth a dozen subjective symptoms,
and this, so far as regards diagnosis, has a large
amount of truth ; but we must recollect that pertur-
bations, which greatly distress our patient, may exist
independently of his chief disease, and it is the patient,
not the disease, that we have to treat. Let me instance
a hypothetical case. A. B. comes to you, and, under
fire of cross-examination discloses that he has had
rheumatic fever some years ago. You examine his
heart and find something wrong with the mitral valve.
You dose him, probably help his heart over its pre-
sumed difficulties with digitalis, and order the inevit-
able belladonna plaster to be applied. But your
patient at his next visit is not a whit better. It was
not his heart which troubled him — that was neither
better nor worse than it had been for many years
past, and was likely to be for many years to come ;
but he suffered from a trigeminal neuralgia, and would
have showered blessings upon you had you relieved
him.

The moral I would point, then, is this : Always

INTRODUCTORY.

commence your interrogatory of a patient by asking
what lie complains of, what are his troubles and
distresses, and if you record his case, write on the
first line, complaint, and give his expressions, as nearly
as possible, with the necessary abbreviations, in his
own words.

Now we come more closely to our subject. The
comprehensive view of what disturbs the equanimity
of a patient, with a view to the alleviation of his
troubles is one thing-, the particular determination of
the physical significance of his ailments, and the pre-
cise diagnosis of his diseases is another. For this latter
purpose, the details of pains and aches, though all due
weight must be given to them, are very deceptive.
How very common it is for a patient to fancy that he
has disease of the heart because he experiences dis-
comfort or pain in the heart-region, and to insist on
being " sounded," so that his doubts may be set at
rest. How rarely do we find that he really has organic
heart disease ? Oftentimes the patient goes away ap-
parently with a look of disappointment that his fears
are not confirmed, and with a doubt probably of our
skill, because his aches are so precise.

In looking over the notes of a hundred cases of the
coarse and decided forms of disease of the heart which
have been under my own immediate care, I find that
in just half the number, there was no complaint what-
ever of any pain referred to any part of the chest.
Seventeen referred the pain generally to the front of
the chest, fifteen to the back of the chest, and especi-
ally between the scapula?. Twelve referred the pain
to the epigastrium ; eleven suffered pain on the left
side of the chest ; whilst two referred their sufferings
to the right side. Those who localised their suffer-

•1

TNTHODUCTORY.

mg-s to the exact area of the heart were hut eight;
and of these, two complained of it only on exertion •
one referred it to the base of the heart ; one described
it as a sense of extreme soreness at the apex ; and in
one, it partook of the character of neuralgia of the left
breast. So far as the evidence derived from the above
cases— which are, I believe, fair specimens of those
presenting- themselves at the public or the private
consulting- room— teaches only eight per cent., or less
than one in a dozen, complain of pain directly referred
to the situation of the organ which is diseased. This
though strange to the non-medical mind, can scarcely
be surprising when we consider that the heart pos-
sesses very little common sensation, and that its
structure can be punctured, torn, or lacerated, with-
out the direct infliction of pain. When we consider
the vast number of patients who present themselves
with symptoms referred to the region of the heart,
but really caused by dyspepsia or pleurodynia, and
then take into account the very small proportion of
real undoubted heart cases presenting signs of local
pain, we must estimate at a very low figure the value,
in a diagnostic point of view, of pain in relation to
heart disease.

Looking on diseases of the heart in general from
the point of view of symptomatology, we find that
their origin and progress are oftentimes very insidious
and obscure. Even* the most pronounced and
dangerous forms of the disease may, in some cases,
go through their stages without betraying themselves
by marked symptoms of distress. This fact was
strongly impressed upon my mind by a case which
was under my care at the North-Eastern Hospital for
Children. A little girl, who had been treated pre-

INTRODUCTORY.

viously for a valvular affection, was brought to me
because the mother thought she seemed a little languid,
though the child complained of no distress On ex-
amination, I found that there was effusion into the
pericardium. She was admitted, and went through
all the stages of pericarditis with extreme distension of
the pericardium, exhibiting one of the most pro-
nounced instances of pericardial friction that I have
ever beard and an accompanying endocardial change,
and yet throughout her whole illness the child com-
plained neither of pain nor distress, and it was impos-
sible to keep her in bed.

There is one form of pain in heart disease, however,
which is of terrible significance — I mean Angina
Pectoris. It has the character of a grip : it shoots
down the left arm and occasionally involves both
arms, or radiates to the back.* This is the pain, mi
generis, of cardiac origin, and if you have once seen a
pronounced example of it, you will never forget it.
The patient suddenly sits up in his bed, and with a
cry of horror indicates his sense of pain at the prag-
cordium. It has great intensity, but is of a cold and

* " The pain of angiua is distinctly located in or about the
midsternum, whence it radiates. Eulenberg says this is due
to the connection between the superior cardiac nerve and
the anterior branches of the four upper cervical nerves ;
while the middle and inferior cardiac nerves are connected
with the four lower cervical nerves, uniting in the brachial
plexus aud first dorsal nerve. The paiu usually runs out at
the peripheral endings of the ulnar nerve, especially the little
finger. It is almost invariably found on the left side only, in
a case where it was on the right side, the pulmonary artery
was the seat of disease."— " Path. Soc. Trans.," 1878. "The
Diseases of the Heart," Dr. Milner Fothergill. Second edition,
London, 1879, p. 285.

INTRODUCTOKY.

sickening character ; the chest is fixed, the breathing
not quickened, and your hand, placed over the epigas-
trium, finds that the heart's action is slow and
laboured. The face wears a look of horror, the hue
is pale or slightly leaden, and a cold sweat breaks out
upon the forehead. Worse than the pain is the feel-
ing- of fearful sinking and depression ; the poor patient
gasps, I shall die !" and, sometimes, as in a case
which it was once my lot to witness, his short, but
concentrated sufferings in a few minutes end in death.
From such a typical case of high diagnostic and prog-
nostic import, there are many gradations of intensity,
until, in some cases, it is difficult to differentiate the
symptoms from those of dyspepsia or hysteria. In some
cases the pain is absent though the other symptoms
are present; such is the "angina sine dolore" of
Gairdner. The points to be remembered are: — (1)
The attacks are paroxysmal with long or short inter-
vals. (2) There is always a sense of coldness experi-
enced, and frequently a cold sweat. (3) The heart's
action is not increased, and (4) The chest is fixed, the
breathing slow.

Few questions in the domain of medicine Wo presented
greater difficulties than that 'of the nature and pathological
significance of angina pectoris. Latham said of it : " We are
sure of what it is as an assemblage of symptoms. We are not
sure of what it is as a disease." In the fatal cases, the lesions
which have been discovered have been various, and in some
no morbid appearances have been demonstrated at all. The
most commonly discovered conditions have been (a) degenera-
tion and calcification of the coronary arteries ; (b) atheromatous
disease of the aorta ; (e) disease of the aortic valves; (rf) fatt3'
degeneration of the muscle of the heart. The affection is
rare, though by no means unexampled, be foremiddle age, and
is much more common in the male than in the female sex. It
has proved fatal even in a tirst attack ; Dr. Arnold, of

INTRODUCTORY.

Rugby, died within three hours of the onset of an attack of
angina pectoris. In the case of a young man, aged twenty-
three (recorded by Dr. John Wilson, Edinburgh Medical
Journal, September, 1874), who died the day after he had
manifested heart-pang, no disease was found at the post-
mortem examination. The heart was flaccid, the cavities
empty, and the valves all healthy. The young man had been
in perfect health until a sudden exposure to cold led up to the
fatal attack. It is obvious, therefore, that we must not look
alone to the post-mortem table for a solution of the difficulties
which beset the pathology of angina pectoris. Fortunately,
cbnical investigation has succeeded in a large measure in
dissipating those difficulties. Dr. Lauder Brunton demon-
strated, in 1866, by means of the sphygmograph, that the
arterial tendon during an attack of angina pectoris is increased.
Dr. Brunton, knowing that the effect of nitrite of amyl
was to relax the arterioles and thus to relieve the tension,
administered this drug by inhalation during the paroxysm of
angina, with complete success ; the symptoms were imme-
diately alleviated. Dr. L. Brunton' s observations have been
conclusively confirmed. More recently, Dr. Murrell has intro-
duced for the treatment of angina pectoris another agent,
which, like amyl nitrite, has the power of relaxing the
arterioles— nitro-glycerine. The use of this drug, which is
administered by the stomach, is also attended by.most obvious
relief of the symptoms. It may, therefore, be taken as
proved, I consider, that angina pectoris is essentially a con-
dition in which the arterioles are contracted, and in which
there is high pressure in the arterial system, and that when
the arterioles are made to dilate, and the intra-vascular
pressure is rebeved, the symptoms abate. You should remem-
ber that angina pectoris is by no means a common affection.
Dr. Hayden, in his large experience, states that he has met
with only six genuine examples ("Diseases of Heart and
Aorta," p. 1043). It follows, therefore, that you must be
careful, in any case which appears to you to present tlie
characteristic symptoms, to discriminate between true angina
and the many forms of pain which are sometimes called false
angina, and which may be neuralgia, intercostal rheumatism,
the consequences of dyspepsia, &c. You will make the
diagnosis by observing whether the symptoms correspond

INTRODUCTORY.

with those I have before described, and especially also by
ascertaining, ,f you have an opportunity of witnessing the
phenomena of an attack, whether the arterial tension during
the paroxysm is increased. On this point you should obtain
the evidence of the sphygmograph if possible. Having recog-
nized your case as one of true angina, supposing that you have
opportunities of further investigation, you will find it in my
opinion, most practically useful to place it under one of
two categories. A, in which the arterial tension is not increased
m the intervals of attacks. B, in which there is persistently
high arterial tension. The cases [A) in which normal tension is
moderate or low, constitute the minority, and for the most part
comprise the exceptional cases occurring in the earlier periods
of life. In such there is an acute supervention of high pres-
sure, the arterioles become contracted (perhaps in obedience
to a direct external cause, such as exposure), the left ventricle
struggles against the difficulty so imposed, and becomes over-
distended. As I have said, such acute angina may be fatal
On the other hand, the paroxysm being relieved, the patient
may go an unlimited time without recurrence. In such cases
there may be no antecedent cardiac disease ; it is not common
to meet with angina in the valvular diseases consequent on
rheumatic endocarditis. I have seen, however, a single
severe attack in a lady aged thirty-one, who presented the
marked signs of mitral regurgitation ; in this case, how-
ever, the sphygmograph demonstrated high tension a
condition quite different to that usually obtaining in such
pronounced mitral regurgitation. In resume, therefore, in
Class A, the angina attack is a neurosis, the essential of which
is the acute supervention of a contraction of the arterioles,
with rise of blood pressure throughout the arterial system,'
and distension of the left ventricle from accumulation of blood
therein. In Class B, which includes the majority of cases of
angina pectoris, the arterial tension is persistently high, though
it is still higher during the paroxysms. In these there is a
special cause for the recurrence of attacks ; such cause is
disease of the coats of the aorta (aortitis deformans) or disease
of the systemic arteries (arteritis) and especially of the
coronary arteries. In such cases you will find the arterial
pulse hard and incompressible, and there will be signs of
hypertrophy of the left ventricle, and probably valvular disease,

INTRODUCTORY.

which is usually aortic. When from any cause the already
high arterial tension is increased, and the left ventricle is
overtaxed in its struggle to propel the blood, angina may
ensue. Undue exertion or effort are frequent exciting causes
of an attack. In some cases, however, paroxysms occur with-
out obvious disposing causes, and in such it seems highly
probable that there is a direct interference with the nervous
mechanism. Lancereaux has described a case which mani-
fested attacks of angina pectoris wherein, at the autopsy,
there was found aortitis, with a direct involvement, by the
disease of some of the fibrils of the aortic and cardiac plexuses
(Cf. Lancereaux, "Anatomie Pathologique," Paris, 1871, p.
257, and Gazette Medicate, 1867, p, 432). Seeing the common
association of the cases of angina which fall under this section,
with disease of the arterial coats, it seems very reasonable to
link the nerve-phenomena with an affection of the sympathetic
filaments which are in such close relation to the coats of the
vessel. If we accept this view, the calcification of the coro-
nary arteries— heretofore supposed to induce the symptoms
through the degeneration of the heart muscle, which, by
impairing the blood-supply, it occasions — is the cause of the
pain rather by the direct implication of the cardiac plexus.
It is quite true that cardiac degeneration follows coronary
obstruction ; but this is a cause, not of the pain, but rather of
the fatal issue. In a case recorded by Romberg, it was proved
that not only the cardiac nerves were involved, but also the
vagus. In his attacks, the patient, a man aged thirty-six,
after a prodroma of apprehension and terror, felt his heart
stand still — there was an intermission of from five to
six beats— at the same time he experienced violent pain on
both sides of the chest, extending to the neck and head.
Here was a complex form of angina, the peculiarity of which
was a long arrest of the heart's action. At the post-mortem
examination the great cardiac nerve was found very distinctly
diseased, and the left vagus as well as the phrenic were
involved in diseased glands. The vagus is the inhibitory
nerve of the heart, and there could be no doubt that an irrita-
tion of its inhibitory fibres produced the long intermissions of
the heart's action witnessed in the case. The high tension
observed in these cases is not necessarily associated with
hypertrophy of the left ventricle. In the case of Dr. Arnold,

10 INTRODUCTORY.

the walls of the left ventricle were much thinner aad softer

atLte? J°Ln ^ed after attlf

ang m pectoris and the heart in his case was found to be very
smaU and its tlssue pale. Dr. W. T. Gairdner says : « ±>0Z

mortem ex^nnnations have generally shown that the heart is
ound fl d ratt rig.dly contractedi andtheIes.ona

found m the muscular substance of the heart itself are usually
such as would confirm the idea of decidedly and permanently
I?}™ , e^'^.rfhert^^ disposition to abnormal con-
traction." The high tension, then, is due to vascular rather
than to cardiac causes ; the left ventricle labours against the
obstacle imposed by the firm contraction of the arterioles. In
the large class of cases of angina pectoris associated with
atheromatous disease of the great arteries, I consider that a
strict analogy is established with those cases of epilepsy which
are found to depend on local irritation of the nerve centres
in the former, owing to irritation of the nerve fibrils involved '
m the wall of the diseased artery, there are periodic explosions
expressed by the tight contraction of the arterioles and the
consecutive heart-struggles, whilst in the latter the expression
ot the maximum of central irritation is an epileptic fit In
any case manifesting angina pectoris, I counsel you strongly
to obtain, by means of the sphygmograph, evidence of the con-
dition of the vessels. I may mention a case in point. I saw
in conjunction with my friend Dr. John Bruntou, an old lady
of sixty-nine, who suffered from severe pain, referred to the
epigastrium and abdomen. This pain might very easily be
referred to visceral congestion, but it was to a considerable
extent paroxysmal, and there was a marked look of anxiety
upon the face with tendency to cold perspiration. The
heart sounds betrayed nothing abnormal, but a tracing of the
radial gave very important evidence. Not only was there
extremely high tension, but the trace bore strongly the
characters of aortic obstruction (see tracing of Aortic Obstruc-
tion in Part II.). I had no hesitation in concluding that the
vessels were extensively diseased, and it seemed to me very
probable that the great suffering referred to the epigastric and
umbilical regions might be ascribed to disease of the coats of
the abdominal aorta. Nitro-glycerine gave relief, and the
subsequent history of the case confirmed the diagnosis. Dr.
Brunton wrote me : " The old lady has gone on tolerably well

INTRODUCTORY.

till two days ago, when failure of pulse came on, only one
decent beat in ten, but over the heart the sounds were quite
normal in strength, rhythm, and note. ... You will find the
case a most interesting witness of the power of the sphygmo-
graph." It is very probable that some of the recognized forms
of abdominal pain are but varieties of angina. Whilst
ascribing, however, to direct disease of the arterial tissues the
causation of a large proportion of those cases of angina which
are accompanied by persistently high vascular tension, I do
not mean to assert that in some instances the attack may not
be initiated by visceral causes. Bergson has narrated a case
of angina, in which there was enlargement of the liver, the
attacks ceasing after treatment directed to the hepatic
disease. (On this as well as many points of interest as regards
angina pectoris, see Dr. Milner Fothergill, "The Heart and
its Diseases." Second edition, chap. xi. London : Lewis.)

You have seen, then, that a large numher of heart
cases occur without the manifestation of any pain-
that the special pain of heart disease, though of great
diagnostic importance, is of comparatively rare oc-
currence. You may he led to inquire what are the
other symptoms that lead up to the suspicion of heart
disease ; and although we cannot enter at all deeply
into symptomatology, we may endeavour to give a
brief answer to the question.

In this review of symptoms, in order to give a
rough idea of the relative frequency, I shall place
between brackets the number of instances in which
each has been observed in the hundred cases which
I have taken as typical. The first class of symp-
toms (A), excluding pain which we have already
considered, includes palpitation and disturbances of
the muscular structure of the heart. Palpitation is
far from being a pathognomonic sign of heart disease.
Its first cause resides often in the nervous system. It
is not by any means a sign of heightened functional

1°

INTRODUCTORY.

activity but is rather the "spurt" of overtaxed and
weaned muscle. Though occurring verv often in
cond.tions in which the heart is not •structurally
diseased, palpitation is a frequent sig-n and source of
trouble m organic heart affections (28) It is
specially called forth on exertion, often of the
slightest degree, and it occasions much distress- in
some cases, especially where the aortic valves cannot
close perfectly, the patients complain that the heart
beats like a hammer. Another sign of imperfect
action of the muscle of the heart is Intermission.
After a number of pulsations at regular intervals, the
heart waits over the whole period necessary for a con-
traction, and then resumes, to wait again after
another interval. Intermittency, like palpitation,
may be no sign of structural heart disease ; it is in
many cases due to an incoordination of nervous
actions, and is to be ascribed, not to cardiac, but to
cerebro-spmal causes. When it does occur, however
m ascertained organic disease, it is of serious import!
It often means that the contraction of the auricles
is at certain times so imperfect that they do not fill the
ventricles. The necessary stimulus to the ventricular
contraction is a sufficient repletion of the cavities.
Hence the ventricles wait until the auricles supply
them with enough blood. A third trouble of heart-
muscle is Irregularity. This, also, is due to a want of
action, in accord, of the layers of muscular fibre of
which the heart consists. The heart does not wait
for a whole beat as in intermission, but alters its
rhythm irregularly. Sometimes the left and right
sides do not contract, or do not complete their con-
traction, at one and the same moment; then the
action may be reduplicate. Sometimes there is so much

INTRODUCTORY.

disturbance that the periods of action and rest cannot
be discriminated ; the beats are tumultuous. Irre-
gularity may, like the other disturbances of heart-
muscle, exist independently of organic disease ; but
when it reaches a high degree, it is one of the
strongest evidences of such disease. Patients some-
times describe the irregular action as like the flutter-
ing of birds. One complained to me of a fluttering
in his heart " like two pigeons." Such signs are of
dangerous import.

The symptoms, however, may be referred, not to
the heart itself, but to the next portion of the system
of blood-distribution— to the arteries. Patients com-
plain of (B) Pulsation. This, we shall see, is very pro-
nounced in the general arterial system when the aortic
valves are incompetent to close. It was complained
of in my patients as a symptom of distress (3) in the
ear whilst lying on the pillow, in the right temple, in
the occipital region. Pulsation is, of course, a cha-
racteristic sign of aneurism, but this condition we do
not intend to discuss. Another arterial symptom in
connection with heart disease, but rare and of no
considerable diagnostic importance, is Flushing. A
very important consequence is (C) Hemorrhage (22).
This may occur from the lungs (12), when it must be
remembered that it has not the dangerous signifi-
cance of the haemoptysis of pulmonary phthisis. Con-
siderable cpiantities of pure blood can be expectorated
with the result of relieving the venous engorgement
of the lung which is the result of some forms of
heart disease. Of worse omen, in my opinion, is the
frecpient voiding of blood-stained sputa; this occurs
usually when the right side of the heart is dilated,
and is one of the late consequences of valvular disease.

INTRODUCTORY.

Bleeding' from the nose (5) is far from uncommon in
heart disease ; haemorrhage may occur also from the
stomach (3), or from the uterus (metrorrhagia) (2).
In all these cases the haemorrhage may occur from the
direct rupture of capillaries by the shock of an unduly
contracting left ventricle, but much more commonly it
occurs from superinduced venous congestion. Occa-
sionally the haemorrhage is not manifest outwardly,
but occurs in the interior of organs.

Other signs are referable to plethora of the venous
system. The veins may sometimes be seen to be
obviously distended, and in some cases, as we shall
describe, the large veins pulsate. Patients with certain
malformations of the heart exhibit a blueness of sur-
face (D), Cyanosis, from the distribution of venous
blood by the arterial channels or from venous con-
gestion. A like blueness obtains intermittingly, on
account of venous congestion, in the paroxysms of
dyspnoea from which patients with heart disease occa-
sionally suffer. A consecpience of habitual venous
plethora may be (E) Dropsy, of which it is well known
that cardiac disease is one of the great inducing causes.

Next in order to the obvious disturbances of the
heart itself and the channels of blood-distribution, we
come to consider the symptoms of disturbance of the
functions of the lungs in heart diseases. These symp-
toms are far more frequent than those referred to the
heart itself. Nearly half the cases (45) complain of
difficulty of breathing. Some (8) are obliged to sit
upright (orthopncea) in order to breathe. A very
large proportion of patients with heart disease suffer
from cough (45).

A great characteristic of the dyspnoea of heart
disease is, that it is produced or aggravated by slight

INTRODUCTORY.

exertion. The heart may fairly accommodate itself to
conditions of rest, hut let exertion call upon it for
increased action, and it manifests its distress by the
imperfect pulmonary circulation, and the consequent
dyspnoea. Or the dyspnoea may be periodic, and not
induced by voluntary effort. Such attacks are called
cardiac asthma. The induced conditions may, how-
ever, be not temporary, but chronic. Persistently
defective heart's action induces persistently defective
pulmonary circulation. The blood tends to stagnate
in the lungs. Chronic bronchitis, and, subsequently,
emphysema follow, and the trouble may be augmented
by oedema of the lungs.

Next we will proceed to notice the Cerebral troubles
which occur in heart disease. These are very com-
mon. The patients complain of languor and extreme
weakness (25). Often the muscular weakness is re-
ferred especially to the arms ; the patients cannot lift
weights as they have been accustomed, and the
muscles feel powerless. They suffer attacks of
giddiness (vertigo) (8), or are subject to fain tings
(syncope) (6). There may be an undefined nervous-
ness (?), with dread of a fit or some calamity, and
lowness of spirits. Headache (5) is sometimes met
with, but is not one of the commonest symptoms.
Trembling of muscles and the irregular jactitations of
chorea (3) are very important to notice. There may
be fits epileptiform (2), or epileptic (2), or various
forms of paralysis may be found. Lastly, there may
be impaired memory and intellectual disturbance of
various kinds. In all cases of heart diseases which
present cerebral symptoms, the fundus of the eye
should be examined by the ophthalmoscope.

The cerebral phenomena observed in heart disease

INTRODUCTORY.

may, for the most part, be divided into three classes.
The first embraces those due to the chronic distur-
bance of balance between the arterial and venous
systems which is the result of imperfection of the
driving- power in the great engine of the circulation.
The brain may suffer from deficient supply of arterial
blood, or from excess of venous blood, or from these
causes variously combined. Arising from these con-
ditions there may be increase of the fluids effused
within the intra-cranial cavities, and degenerations of
brain tissue, owing to the impaired nutrition.

The second class of cerebral phenomena occurring
in heart disease includes those due to intra-cranial
hemorrhage. You must remember that apoplexy is
to be feared in cases of hypertrophy of the left ven-
tricle of the beart, the strong muscular contraction
distending the arterioles and capillaries to the point
of rupture. It is much more to be feared, however,
when tbere are heart hypertrophy and kidney disease
combined. In such cases there is not only excess of
driving power, but the arterioles have suffered
change — they have become brittle and prone to rup-
ture. Out of twenty-two cases of apoplexy, Kirkes
found thirteen accompanied by hypertrophy of left
ventricle, and fourteen accompanied by renal disease ;
and Eulenberg, in six cases of apoplexy, found five
with contracted kidney and heart hypertrophy.

The third class includes the interesting phenomena
now known to be due to the sudden blocking of a
cerebral artery by a morsel of coagulum detached
from a diseased portion of endocardium, and swept
onwards in the blood current until it happens to be
arrested in an arterial channel which it is too large to
pass through.

INTRODUCTORY.

The straightest course which such a plug' can pursue
is from aorta to middle cerebral artery of the left or
the right side, and the symptoms produced are hemi-
plegia, with coma, or aphasia. Sometimes, however,
the effects are more chronic, the plugging of the cere-
bral vessel, and hence the cutting off of nutrient
supply, inducing softening of that portion of the
brain supplied by the vessel.

Instead of a large plug of this sort, we have reason
to believe that small ones which are arrested in the
cerebral arterioles occasionally occur, and may ac-
count for symptoms for which no cause has been dis-
covered. Thus in chorea, which has a notable con-
nection with disease of the heart, it has been suggested
by Dr. Hughlings Jackson that there are embolisms
of the arterioles of the corpus striatum and the
adjoining convolutions.

Emboli may be carried in the blood current to other
parts than the brain; the spleen, liver, and kidney can
be thus affected. Capillary embolism of the kidney
is probably by no means uncommon. It is suggestive
that in two or three cases I have noted, in which
chorea occurred in rheumatic endocarditis, frequent
micturition was a symptom complained of. Or
from the right cavities plugs may be detached and
carried into the pulmonary artery, plugging some of
its branches in the lung. From this result the
appearances which used to be called "pulmonary
apoplexy."

We turn now to another set of symptoms in heart
affections, those of the stomach. Pain referable thereto
we have already noticed. A large proportion of
patients with heart disease complain of some of the
symptoms of indigestion — gastric catarrh is common ;

C c

INTRODUCTORY.

nausea, vomiting-, pyrosis, and flatulence are frequent,
and occur in a circle, the heart trouble occasioning
them, and the symptoms reacting- to cause palpitation
and heart distress. The other abdominal viscera also
partake of the venous plethora induced in heart
disease. Haemorrhoids are frequently met with.

Another set of symptoms in diseases of the heart
comprises those referred to the throat. This subject
presents, in my opinion, a wide and very promising-
field for observation. Pain beginning- at the throat
is referred to by some as a very dang-erous sig-n in
these affections. There are many instance on record
in which a patient has grasped at his throat, evincing-
signs of acute pain, and has shortly afterwards ex"
pired. The sudden throat pains in heart disease are,
I believe, for the most part, varieties of angina, and
may be discriminated by the rules I have given.
Other forms of pain of less laryngeal character and
of less intensity are, however, met with, and these are
usually accompanied by flatulence and dyspepsia. The
"rising in the throat," unaccompanied by pain, is
usually either dyspeptic or hysteric. Next to the
throat-angina, the symptoms of greatest interest and
importance are loss of voice (1) and hoarseness (4).
The case of aphonia which I have noted, occurred
during the progress of pericarditis— to what was it
due ? A case which suggests an answer to this ques-
tion is given by Dr. Morell Mackenzie in his book on
" Hoarseness and Loss of Voice." In this instance
pericardial effusion was accompanied by aphonia due
to paralysis of the abductors of the- vocal cords.
After the cessation of the pericarditis, the mobility of
the affected laryngeal muscles returned. The patho-
logical process whereby such paralysis is brought

INTRODUCTORY.

about is yet undiscovered. We find that hoarseness
occurs as a symptom of aortic aneurism, the disposing
cause in such case being- pressure of the aneurismal
sac on the left recurrent nerve, inducing- paralysis of
certain of the laryngeal muscles. I have not found,
as far as my own experience goes, that hoarseness is
prone to occur in aortic valvular diseases. The car-
diac conditions accompanying hoarseness I have
found to be disease of the mitral valve, with which
broncho-pneumonia, or some other form of pulmo-
nary mischief, co-exists. Unilateral paralysis of the
intrinsic muscles of the larynx is frequently met
with in local disease of the pulmonary texture.

Disease of the Mdneys may stand as to disease of
the heart in a, threefold relation. The latter may be
cause, consequence, or concomitant. The renal dis-
ease may be (a) directly caused by the heart-imper-

'• fection. Tlie kidneys, like the other viscera, suffer
venous engorgement, and, if this be long continued,

'a low form of inflammation, attended with increased
formation of fibrous tissue, may occur in them. In
the earlier stages such a state of things is indicated
by albuminuria, in the latter by the detection of
kidney tube-casts in the urine by the microscope.
But (b) the heart disease may be primarily caused by
the renal disease. When, owing to structural disease,
the kidneys are unable to excrete from the blood the
urinary solids, the natural consequence is the reten-
tion in the circulation of effete material. It is sup-
posed that this material perfunctorily retained, so
irritates the arterioles, or the vaso-motor centre
which o-overns them, as to cause them to contract.
Such contraction (it seems to me that the term
" spasm," which has been used in respect of this

~u INTRODUCTORY.

effect, is misapplied) being' long- kept up, the result is
the same as occurs in overtaxed muscle- tissue gene-
rally—viz., hypertrophy ; so there is induced a peri-
pheral obstacle to the onward current of blood in the
arteries. The heart struggles against such an ob-
stacle, and its efforts produce hypertrophy of the left
ventricle. Thus, hypertrophy of the left ventricle
may even be induced subsequently to renal disease
in children. Or it may be (e) that the heart disease
and the kidney disease are both effects of one cause.
The form of kidney disease which usually accom-
panies cardiac hypertrophy is what is called " con-
tracted kidney ; " this is for the most part associated
with some gouty affection. We know that in gouty
disease the blood is impure, and it is supposed that
such condition gives rise to a disease of arteries and
capillaries generally throughout the system leading
to thickening of their walls, but not necessarily nor
wholly of the muscular part thereof. The heart
hypertrophies because it struggles against the ob-
stacle, not of arterioles actively contracting, but of
arterioles which have undergone degeneration,
whereby their walls have become thickened and in-
elastic. The capillary circulation is thus rendered
slower, and the heart muscle becomes stronger to
overcome the impediment so produced. The kidney
is diseased because its vessels are involved in the
general disease. The rules you can deduce from a
consideration of the whole subject are : 1. In cases
of cardiac disease carefully examine the condition of
the urine. 2. When you find renal and cardiac
disease co-existing, weigh carefully the facts of the
previous history, and endeavour to find out which
pathological condition preceded the other.

INTRODUCTORY.

I turn now to another branch of the subject. I
have said that the symptomatology of heart disease is
often obscure. We find that its etiology is often
obscure likewise.

There are' two errors, in my opinion, into which
many are prone to fall. The first is that valvular
disease of the heart is rarely found except as a conse-
quence of rheumatic fever ; the second that there is
danger of heart-complications in the severer forms of
rheumatism only. Let us turn to the records of
actual cases. Taking seventy-seven of the hundred
cases before cited, in which the early histories are
sufficiently precise, I find that thirty-four occurred
in those who had suffered one or more attacks of
undoubted rheumatic fever ; but in thirteen there
had been rheumatic pains only, not sufficient to keep
the patients to their homes ; and in fifteen there was
no history of any rheumatic affection whatever, and
only, if any symptoms at all, those of a lightly-
regarded indigestion. Rheumatic gout had been
suffered by two patients, scarlet fever by three, and
typhoid, or " low" fever, by four. Typhoid fever is
not attended by valvular disease, but by such an
enfeeblement of the muscular walls that dilatation
may ensue. In six cases the evidence pointed to the
conclusion that the disease was congenital. You will
conclude, therefore, that, though it is (1) pre-
eminently necessary that you should carefully ex-
amine the condition of the heart in any patient
who is suffering from, or who has suffered from
rheumatic fever, it is important to do so also in (2)
those who have been subject to slight forms of
rheumatic pain, and that (3) there is a large
remnant recpiiring careful exploration whose diseases

INTRODUCT<"'HY.

are not to be traced to any obviously rheumatic
condition.

Excluding, then, those I have mentioned, what are
we to look for as the most common causes inducing
heart disease ? I will briefly enumerate some of
them: Over-exertion and muscular strain— alcoholic
indulgence — syphilis — tuberculosis— the puerperal
state — poisoning by phosphorus — lead poisoning —
imperfect and improper . nutrition— disease which
involves the structures contiguous to the heart and
pericardium — disease which induces venous engorge-
ment of the lung, whence distension, dilatation, an
hypertrophy of the right side of the heart.

\ ou may, from a general consideration of this in-
troductory chapter, obtain in some degree an answer
to the question which you will probably propound: —
Under what circumstances of symptoms and previous
history is it necessary for me to make a physical ex-
amination of the heart-region ? There is one aphorism
which I would impress on you, however, which covers
the whole ground. It is this, that you have never made
a complete examination oj any -patient, whatever be his ail-
ment, unless you have estimated, as far a's possible, the con-
dition of his heart.

We shall now consider the mode of doing this. We
pursue the investigation through our senses of sight,
touch, and hearing. We do not grope for one sign
which, when found, shall be conclusive to us ; but
after we have obtained all the evidence presented to
our senses, our logical faculty must discriminate and
lead us to the truth. We work by no single method,
but by a combination of methods and modes of thought.

L'3

LECTURE II.
INSPECTION.

Cyanosis temporary and permanent— Pathological causation-
Chilling of finger-tips — Clubbing — Ansenaia — Graves'
Disease— Sub-icterus— Arcns senilis— Cardiac dyspnoea—
Orthopncea — Decubitus in pericarditis — Cheyne- Stokes'
dyspnoea— (Edema— "Venous turgescence— Venous pulsation
—Visible arterial pulsation— Locomotive pulse— Apex-beat
— Area of visible cardiac impulse.

You may take it as an aphorism that you can never
make a satisfactory examination in suspected heart
disease, unless your patient be stripped to the 'waist.
Very valuable evidence is afforded by inspection.
The first point you will probably note is the general
hue of the surface.

We will suppose that there is (A) a marked blue-
ness of the surface. You will elicit whether this is
temporary, sometimes passing- away altogether, or
permanent, varying perhaps in intensity, but never
quite disappearing. The temporary blueness will be
associated, probably, with attacks of cardiac asthma,
of which dyspnoea is the great feature. The perma-
nent blueness may also depend on the same cause as
the temporary — viz., undue fulness of the venous
system. In such case you will find respiratory
trouble — bronchitis or emphysema or both accom-
panying it — and it affords strong presumptive

INSPECTION

evidence of dilatation of the right cavities of the
heart.

There is a form of blueness dependent on malfor-
mation of the heart so special that it constitutes the
chief sign of, and gives a name to, the affection. Such
is blue disease, morbus cteruleus, or Cyanosis. Here
you find a deep discoloration, in some cases approach-
ing- a black, involving- all the surface, but especially
manifest in the lips and the mucous membrane of the
mouth. The colour is persistent, but is deepened
when breathing- and the heart's action are quickened,
or when coug-h comes on. You will scarcely find any
difficulty in recognising- this condition— the hue is so
characteristic ; it is more pronounced and more
g-eneral than that which obtains in ordinary venous
congestion. Moreover, you will elicit perhaps that
the affection dated from birth. If so, the evidence is
nearly conclusive, but, if not, the diagnosis is by no
means set aside, for the discoloration may not be
obvious until periods remote from birth. Most pro-
bably, however, your patient will be an infant or
young child. Nearly half the cases of this affection
die before they are a year old • two-thirds before they
are two years old ; and though a few instances are
recorded in which adult life has been attained, they
are very rare.

We may now inquire, what is the pathological sig-
nification of the phenomenon 1 As a matter of fact
in a case of cyanosis the chances are rather more than
ten to one that there is an abnormal communication
between the right and left cavities of the heart, either
between the auricles, owing to patency of the foramen
ovale or between the ventricles, owing to imperfection
of the inter-ventricular septum. Furthermore, the

INSPECTION.

chances are about six to one that the pulmonary artery
is obstructed. The cause of the blueness, according to
John Hunter, was the admixture of venous and arte-
rial blood in the circulation. This explanation seemed
simple enough. Owing to the structural defect in the
heart, the dark- coloured venous blood mixed with the
arterial, and the resulting darkened compound was
propelled through the systemic arteries. This theory
has been opposed in modern days, but it appears tome
that its opponents try to prove too much. At any rate
they hold that the explanation given above is not the
true one of the cyanosis. According to them, cyanosis
is due to congestion of the venous system, and this
congestion is the result of obstruction of the pulmonary
artery, or of some other malformation which induces
an obstacle to the return of blood from the systemic
veins. Premising that, in my opinion, the truth lies
between these two theories, we will examine each of
them.

The theory that the blueness results from direct
mixture of venous with arterial blood, at first sight
appears very plausible. Out of one hundred and
ninety-five cases recorded by Stille and Peacock, one
hundred and seventy-eight presented abnormal com-
munication between the right and left sides of the
heart ; admixture of venous and arterial blood there-
fore is possible and likely, and often inevitable. The
hue of the patients is just that of those in whom venous
blood is circulating : you see it in cases of impending
suffocation; you may have many opportunities of
witnessing it during the administration of nitrous oxide
gas, when the blood is rendered of the venous colour
by the excess of carbonic acid which it cannot get rid
of. What are, then, the objections to the theory ?

INSPECTION.

The first objection is afforded by the anatomical excep-
ts Seventeen of the cases recorded presented no
possibility of the arterial and venous currents abnor-
mally commingling. This is .sufficient to prove that
tlie cyanotic tint cannot be always due to the arterio-
venous anomaly. The second objection is that we can
have communication between right and left heart with-
out the appearance of cyanosis. This does not seem
to me a fatal objection. The question is one of deo-ree •
the tint of the arterial blood may mask that of the
intermixed venous blood, or vice versa. Nay, more, a
patient having this anomaly may present the peculiar
coloration at one time and not at another. You may
understand this by observing the differences in hue of
a woman in health and in a state of amemia and
chlorosis. Let the blood corpuscles be numerous and
healthy, and they would mask the coloration due to
venous admixture, but let them be by any cause
diminished in number or in colour, and the dark tint
would declare itself.

Now let us turn to the other theory— that the color-
ation is alone due to venous congestion. The anato-
mical argument weighing with those who uphold this
theory is, that obstruction of the pulmonary artery is
an important and frequently-observed condition in
cyanosis even when there is communication between
right and left heart. But by their own data it is
shown that this sign is less constant than the arterio-
venous communication, the chances of the first condi-
tion being about six to one, the chances of the second
more than ten to one. Moreover, it is an ascertained
fact that there may be great obstruction of the pul-
monary artery without cyanosis. A case under my
care at the North-Eastern Hospital for Children

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showed this most positively. A little girl, aged eight
years and a half, presented signs of extreme ansemia ;
there was no blueness, but great pallor ; all over the
heart region was heard an extremely lond murmur
with the first sound ; it was loudest at the base of the
heart. At the autopsy we found that there was
obstruction by narrowing of the pulmonary artery.
This was the only morbid condition to account for
the murmur. It is evident, then, that there can be
great obstruction of the pulmonary artery without
cyanosis. It is, however, undoubtedly true that
iii some cases of blue disease, there has been found no
communication between right and left heart, but only
an obstruction upon the venous side which has given
rise to a general congestion of the veins of the
system.

From these considerations I think we are justified
in arriving at these conclusions — first, that in a large
number of instances of congenital cyanosis there is
abnormal communication between right and left
heart, and it is scarcely reasonable to doubt that the
circulation of venous blood with the arterial tends to
produce the peculiar blue coloration ; secondly, that
in some cases the blueness is produced only by undue
fulness of the superficial veins. We know that such
blueness can be thus produced, because we see it
during attacks of dyspnoea, which spring from many
causes, and we are familiar with it when severe cold
affects the surface of the body. In this latter condi-
tion the cold causes contraction of the arterioles, and
the blood is retained in the capillaries and venous
radicles.

Having recognised your case as one of congenital
cyanosis, you are by no means to stop here, but to

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examine by all the methods which will be detailed
hereafter in order to determine, as far as possible,
whether there be any cardiac malformation, and if so
what is its nature. For cyanosis may occur from
causes which affect not the heart, but the lun-s
Any cause which considerably impedes access of air
to the lungs or seriously diminishes the extent of
breathing surface, may induce cyanosis. You must,
therefore, in these cases, carefully investigate the
pulmonary as well as the cardiac conditions.

There is one point in cases of venous obstruction
from any cause which may be classed under minutiee,
but which is of considerable diagnostic importance— :
the condition of the finger-ends. Notice if the
finger-nails are blue in colour. If they are per-
sistently blue, you may conclude that there is per-
sistent fulness of the venous system. If they are
occasionally blue, you will find the blueness coinci-
dent with attacks of dyspnoea. Notice also the
temperature of the finger-ends so far as it is manifest
to touch. Coldness means great defect of circulating
power. Blueness and coldness together constitute a
measure of the danger of attacks of cardiac asthma,
and when these signs are persistent in cardiac disease,
they show that the end is not far off. Notice next
the shape of the finger-ends. When the return of
blood from the veins to the right heart is obstructed
to a considerable degree and for a protracted period,
the finger-ends become thickened at their extremity,
or clubbed. Dr. Dobell considers that when there is
symmetrical clubbing of the finger-ends, and the
nails are of the normal shape, the chances are in
favour of heart disease ; when the clubbing is
attended with curvature of the nails over the ball

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iormed by the finger-tips, the chances are in favour
of phthisis. The reason, probably, is that in the one
case the adipose tissue exists in its normal quantity,
and in the latter case it has wasted, just as in phthisis
all the adipose structures waste.

We will now turn to another branch, and suppose
that our patient does not present blueness but (B )
pallor. The skin, the mucous membrane of the lips,
the gums, and the conjunctival surface of the eyelids
are pale ; the sclerotic portion of the eyeball is of a
pearly white. The patient, you say, is bloodless—
ansemic. Anjemia may simulate heart disease, may
be produced by heart disease, may aggravate heart
disease. The method of differential diagnosis between
the heart disturbances induced by antemia and by
organic heart disease respectively, we shall hereafter
consider, but there are two conditions of anaemia
which we may with advantage notice here.

The first is the condition of pallor associated with
renal disease. We have seen in our introductory
lecture that there is an especial relation subsisting
between cardiac and renal disease. It is most im-
portant to discover such co-existence. If, in addition
to pallor, you notice a " puffing" beneath the eyelids,
or other signs of oedema about the face, you may
suspect renal complication, and prepare (1) to ex-
amine the urine, (2) to use the ophthalmoscope. You
will determine the specific gravity of the urine, ascer-
tain whether it is albuminous and examine its sedi-
ment by the microscope. You will examine the
fundus of the eye to ascertain whether certain changes
which are known to co-exist with albuminuria are
present. The red field of the fundus oculi presents
in albuminuric retinitis irregular, or star-shaped

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black and white patches, often glistening and pre-
senting- a metallic lustre, with, sometimes, dots of
apoplectic extravasation.

The next condition usually, if not always, asso-
ciated with anaemia, which we shall consider, is known
as Graves' or Basedow's disease. This peculiar
affection, by a strange displacement of an adjective,
has been called exophthalmic goitre. It is charac-
terized by a triple sign ; (1) prominence of the eye-
balls; (2) enlargement of the thyroid body; "(3)
irritable action of the heart. The affection is met
with much more commonly in women, and between
the ages of twenty and forty. The prominence of
the eyeballs (exophthalmos or proptosis) is readily
distinguished. The globe seems to be pushed for-
ward in varying degrees from what seems merely an
unusual size of the eyeball to a most unnatural pro-
trusion—to such an extent that the eyelids cannot
cover the globe, and the cornea becomes dimmed by
inflammatory changes. The thyroid enlargement
varies much in degree. In the cases I have seen, it
has not been symmetrical ; of three cases the en-
largement was chiefly of the right lobe in two. The
swelling is elastic to the touch, and pulsation of the
arteries is readily felt. Care must be taken to dis-
tinguish it from aneurism. Dr. Stokes has mentioned
a case in which such a mistaken diagnosis was made,
and a day actually fixed for the performance of the
operation of deligation of the carotid artery. The
beating of the heart is visible over a wide area ;
the action is very rapid, excited by the least emo-
tional provocation, and often exceeding 120 per
minute. This affection does not rank as a heart
disease, but it may lead to h}rpertroplry and dila-

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tation. It is really an affection of the sympathetic
nerve.

This strange disorder may be induced by causes operating
on the nervous system. Trousseau has recorded a case in
which its three symptoms were developed in a single night from
excessive mental emotion. Milner Fothergill also has men-
tioned an instance of its sudden occurrence after emotional
shock. Dr. Lauder Brunton considers that the palpitation
characteristic of the disease is due to direct stimulation of the
accelerator cardiac nerves which proceed from the vaso-motor
centre in the medulla oblongata, accompany the vertebral
artery, and, after passing through the inferior cervical ganglion
of the sympathetic, are supplied to the heart. Irritation of the
inferior cervical ganglion would account for the cardiac excite-
ment. The thyroid signs are explained by paralysis of the
vaso-motor nerves of the thyroid, which are derived from the
same ganglion. Such paralysis causes dilatation of the small
arteries at the back of the eyeball ; so the globe is pushed
forwards, the degree of prominence varying with the amount
of dilatation of the vessels. In some fatal cases, implication of
the sympathetic nerve has been proved to demonstration. In
one instance its ganglia in the neck were found atrophied
almost to extinction. In another case, the middle and inferior
cervical ganglia were enlarged, hardened, and infiltrated with
granular matter, the sympathetic nerve itself being involved
in the morbid change. (See "Diseases of the Heart," by Dr.
Hayden, p. 1061.) More recently Dr. Shingleton Smith, of
Bristol has described a very importaut case ( Medical Times and
Gazette, 1878), in which there was entire destruction, by disease,
of the inferior cervical ganglion on the left side of the neck.
The ganglion had become completely atrophied, "its place
being occupied by an inert mass of calcareous matter and
fibrous tissue."

We will now suppose that our patient presents
neither blueness nor pallor, but (C) a yellowish tinge of
the surface. Deep jaundice is not frequent in heart
disease, but a slightly icteric hue of the face, with a
more deeply-tinged conjunctiva where it covers the
sclerotic, is not uncommon in the later stages of

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valvular disease when passive congestion of the liver
is one of the trouhles. When you find your patient
past the prime of life, the victim perhaps of alco-
holism, with a generally dusky j^ellowness of the
skin, but without jaundice, the surface of the body
somewhat greasy to the touch, the muscles felt to be
flabby and found to be weak, patches of dilated capil-
laries upon the face, and venous turgidity of the
conjunctiva — when, moreover, you notice that breath-
lessness or faintness is produced on exertion — you
may fear fatty degeneration of the heart. For the
diagnosis of this affection one sign has been ad-
duced especially, and has perhaps sometimes been too
strongly relied upon — the presence of an arcus senilis
in the cornea. This requires careful scrutiny, for
there are arcus and arcus. Near the junction of
cornea and sclerotic, where the former should be clear
and transparent, you may see a circle, a semicircle, or
a crescent of opaque whiteness. If this be well
defined, and the rest of the cornea bright and trans-
lucent, it is, probably, no indication of serious in-
ternal degenerative change. The corneal opacity is
probably due to fibrous proliferation or calcareous
infiltration. But if the ring be ill- defined, rather
yellowish than white, the rest of the cornea being
slightly cloudy, you may consider that the chances
of cardiac defeneration are formidable.

Having learnt the lessons to be deduced from the
complexion and hue of our patient, we will next con-
sider the points to be gained from observing his mode
of breathing and the postures which he assumes. In
this section we will consider first cardiac dyspnoea.
As I have said in the introductory lecture, this symp-
tom is especially provoked by exertion. Thus it differs

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from dyspnoea of pulmonary origin. You may find
your patient breathe easily enough if he has been
still for a short time previously to your examination,
but if you call upon him to walk briskly for a few
minutes, or especially if he ascend a few stairs,
breathlessness comes on. This dyspnoea is peculiar —
there is no real obstruction either to inspiration or
expiration, but the patient gasps restlessly, there is
an instinctive craving for more air to oxygenate the
sluggish blood in the lung ; there is air-hunger as the
Germans expressively term it. Such is the dyspnoea
of the earlier stages of valvular imperfection ; but in
the later stages the symptoms may be far more dis-
tressing. The sign which especially distinguishes
the dyspnoea of the later stages of cardiac disease is
orthopnea — the patient cannot lie down ; perhaps
can scarcely recline from the perfectly upright posi-
tion : the whole mental energies seem bent upon the
one task of getting air into the chest. For a descrip-
tion of the most extreme condition of cardiac dyspnoea,
I will quote the graphic words of Hope. The
patient, " incapable of lying down, is seen for weeks,
and even for months together, either reclining in the
semi- erect posture supported by pillows, or sitting
with the trunk bent forwards and the elbows or fore-
arms resting on the drawn-up knees. The latter
position he assumes when attacked by a paroxysm of
dyspnoea; sometimes, however, extending the arms
against the bed on either side to afford a firmer
fulcrum for the muscles of respiration. With eyes
widely expanding and starting, eyebrows raised, nos-
trils dilated, a ghastly and haggard countenance, and
the head thrown back at every inspiration, he casts
around a hurried distracted look of horror, of anguish,

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and of supplication; now imploring in plaintive
moans or quick, broken accents and half-stifled voice,
the assistance already often lavished in vain; now
upbraiding- the impotency of medicine, and now, in
an agony of despair, drooping his head on his chest,
and muttering a fervent invocation for death to put a
period to his sufferings." When the conditions of
cardiac dyspnoea have long continued, you may find
a new condition established, more merciful, but of
even more fatal augury — carbonic acid poisoning.
The blood is deteriorated by the carbonic acid, of
which the respiratory effort is powerless to disem-
barrass it. The patient is in a constant state of drowsi-
ness, with difficulty aroused, but waking in distress
every now and then wben the instinctive craving for
more air asserts itself. In the end coma supervenes.

Such are the modes of comportment in chronic
diseases of the heart wherein dyspnoea is a feature.
In some cases of acute pericarditis you observe no re-
spiratory trouble. Your patient usually lies upon
his back, sometimes desiring that his head and
shoulders should be raised ; if he turns, be prefers to
lie upon bis right side, because when on his left side
there is not only more direct pressure upon the peri-
cardium, but the liver tends by its weight in this
position to press upon the heart. It is usual in peri-
carditis for a patient to be very unwilling to change
his position ; syncope may be easily induced by rough
movements, and it is to be remembered that such
syncope may be fatal. The expression of counte-
nance in pericarditis is often that of anxiety and appre-
hension, and wandering of the mind is common.
Dyspnoea, such, as we have described in relation with
chronic heart disease, may occur in pericarditis, but

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you must not look for it as a common symptom. It
occurs when the fluid effused into the pericardial sac
mechanically obstructs the action of the heart, or in
cases where a less amount of effusion weakens an
already weak heart.

The " reason why" of all the forms of cardiac
dyspnoea is not very easy to trace. In some cases
the desire for the upright position is probably due to
the relief from the pressure that the diaphragm, im-
pelled by the abdominal viscera, occasions upon the
right ventricle which such position induces. In
others, where there is fluid in the pericardium, this
relief is enhanced by the gravitation of this fluid to
the most dependent parts of the pericardial sac, and
thus the easing- of the heart-muscle from pressure.

A characteristic form of rhythmical dyspnaza is occasionally,
though rarely, observed. In such cases there are alternating
periods of arrest, and of excitement of respiration. In the
former period the thorax is absolutely motionless, and the
patient appears almost as if dead. Then a faint wave of inspi-
ration is noticed, followed by other respiratory efforts shallow
and slow. The succeeding respirations become gradually
deeper and quicker, until the chest is agitated with severe
dyspnoea ; then, arrived at its maximum, the paroxysm abates,
the retrocession being as gradual as the onset, and at the end
there is a period during which breathing is iu complete arrest.
This form of dyspnoea has been called after those who first
observed and described it Cheyne-Stohcs' respiration.
Dr. Stokes termed it " respiration of ascending and descend-
ing rhythm." The periods during which respiration is sus-
peuded usually last from a quarter of a minute to half-a-
minute, whilst the periods of rise and fall of respiration are
of abuut the same (or rather longer) duration. In some cases
arrest has been for only ten seconds, and respiration for
seventy-five. The greatest duration of periods which I have
found recorded is in a Memoir by Prof. Sacchi (" Riv. Clin, di
Bologna," Feb. 1877, pp. 33-47). Here the respiratory arrest

D 2

IxN'SPKCTION.

and the dyspnoea each lasted for two minutes. When this
peculiar symptom was first observed, it was supposed to
directly mdicate a condition of disease of the heart, especially
tatty degeneration; further observation showed, however,
that such disease was by no means necessary for its produc-
tion. Then it was thought to be causally associated with
dilatation and loss of elasticity in the aorta. Now that atten-
tion has been more fully called to the symplom, however, a
numerous array of cases shows that this association also can-
not be upheld. The symptom has been observed in cases which
at first sight seem very diverse, but which can, I think, be
conveniently divided into three categories. 1. Cases attended
with cerebral lesions— viz., cerebral haemorrhage, tumours,
uraemia, shock from surgical injury, alcoholism, acute renal
disease, tubercular meningitis. 2. Cases attended with lesions
of heart and great vessels— viz., fatty degeneration, pericar-
ditis, atheromatous disease of aorta, aortic aneurism, valvular
disease (double aortic with mitral insufficiency, mitral stenosis
dilated aorta co-existing, aortic regurgitation and obstruction),
sclerosis of coronary arteries. 3. Cases of certain acute
febrile diseases— viz., diphtheria (Hutterbrenner), typhoid
fever (Wharry). A large majority of the cases occur in the
male sex ; for the most part the age is over fifty, when dege-
nerative diseases are common, the exceptions being in the
acute diseases which I have noted. The sign is one of extreme
danger; the cases, with very few exceptions, have been fatal.
The question as to the causation of this peculiar rhythmical
dyspnoea is a very difficult one. The most plausible theory
was first propounded by Tranbe. He considered that the
conditions giving rest to the symptom have one feature in
common— they impair the due arterialization of the blood
supply to the nerve centres. You will realize that this would
be the effect either of the direct impairment of the heart-
muscle, or more indirectly of the cerebral lesions. As regards
the latter, it is to be noted that the symptom seems to be
allied with causes that induce compression in the neighbour-
hood of the medulla oblongata (Cf. Guttmann " Handbook of
Physical Diagnosis," Sydenham Society's Translation, p. 55).
According to Traube's theory, then, the inadequate arteriali-
zation of the blood lowers the irritability of the cerebral centre
which presides over the respiratory movements. In physiological

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conditions this centre is called into activity by the accumu-
lation of carbonic acid in the blood ; when, owing to condi-
tions of disease, the irritability of the centre is materially ■
lessened, it follows that a much greater than normal accumu-
lation of carbonic-acid is necessary to rouse it to action. In
a case, therefore, which manifests Cheyne-Stokes' respiration,
the first thing which occurs is the establishment of a condition
of impaired irritability of the respiratory centre (this by
Traube's theory through mal-oxygenation) ; the long respi-
ratory arrest gives time for the accumulation of carbonic-acid
in excess in the blood; arrived at a certain maximum, this
begins to stimulate, slowly and imperfectly at first, and after-
wards in increasing degrees, the centre, so that it develops
the respiratory efforts till they culminate in dyspnoea. Then,
as the centre ceases to be stimulated, or becomes exhausted,
dyspnoea again supervenes. To this theory Filehne has
instituted objections, but these rather go to modify
and amplify than to destroy it. He would ascribe the
phenomena to impaired coordination between the respiratory
and the vaso-motor centres, the former must be less excitable
than the latter. His theory is thus expressed by Gutt-
mann:— At the end of the respiratory pause there is a large
disappearance of oxygen from the blood, carbonic acid has
accumulated, the vaso-motor centre is thereby stimulated, and
the arteries (the cerebral arteries amongst the rest) at once con-
tract; this produces a gradually- increasing anemia of the respi-
ratory centre, and inspiration becomes more and more deep; this,
however, supplies the wonted oxygen to the blood, the arterial
spasm is relieved, the anaemia of the respiratory centre passes
off, and with it the exaggerated impulse to respiration, and
breathing once more becomes superficial. When the arterial
spasm has entirely subsided, so that the respiratory centre is
abundantly provided with decarbonized blood, the stage of
apnoea, the pause, is reached, and lasts till, by the abstrac-
tion of oxygen from the blood, the irritation of the vaso-
motor nervous centre is renewed, and the whole series of
operations again gone through. That the arteries are strougly
contracted is proved by the increase of the arterial tension and
of the blood-pressure, while the aua?mic condition of the brain
is demonstrated by the fact that in young children, at the end
of each respiratory pause, immediately before the recommence-

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ment of respiration, and also while inspiration is gaining in
depth, the great fontanelle is depressed. And, further, this
• form of dyspncea may invariably be arrested at the very com-
mencement of each seizure by the inhalation of nitrite of amy],
which dilates the vessels (lor., oit, p. 50). The occurrence
under my care of a typical case has given me close opportunities
of studying the phenomena which we are discussing. In my
case the symptoms developed simultaneously with an attack
of right hemiplegia and aphasia. The attack was proved to be
due to disease of many branches of the cerebral arteries, espe-
cially the middle cerebral of the left side, and there was'mueh
disorganization of brain-tissue, the morbid changes approach-
ing close to the medulla oblongata. The heart and aorta were
perfectly healthy. In the first case recorded (by Dr. Cheyne)
there was, in like manner, right hemiplegia and aphasia. Dr.
Broadbent has recorded a case in which there were tbe same
paralytic lesions due to cerebral hemorrhage. Mr. Frederick
Treves has described a case in which the phenomenon super-
vened on the shock of an injury— comminuted fracture of the
leg, amputation : in this instance, also, there was no cardiac
lesiou. It can scarcely be doubted, that at least in certain cases
the symptoms can be developed by cerebral and not cardiac
causes. The theory, therefore, which ascribes its cause to an
induced anemia of, or a defective circulation in, the respiratory
nerve-centre, necessarily fails. In my case, the sphygmograph
showed that both volume and tension in the arteries v. ere good
and above the normal (see Part II.). There is, however, but
little difficulty in concluding that in these cases the respiratory
nerve centre is directly influenced — that it suffers a paralytic
lesion, and so its irritability is impaired. This could be
accomplished by the contiguity of disease or by shock. The
acute diseases — typhoid fever and diphtheria — in which the
phenomenon has been noted, are both occasionally attended
with cerebral implication and paralysis — in such cases where
the symptom supervenes, it may not unreasonably be ascribed
to a paresis of the respiratory centre. Still, it may be doubted
whether, in some cases, the symptom may not be initiated by
disease of the heart-muscle itself. A review of the recorded
cases seems to afford no positive evidence that it can be so
initiated, for those in which degeneration of heart has been
described have been almost invariably associated with disease

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of the great vessels. Dr. Bradbury has recorded a case asso-
ciated \ith fatty degeneration of the heart, but here the
occurrence of syncopal convulsions showed the implication ot
he central nervous system. It is evident that the phenomenon
is by no means to be interpreted as a sign of fatty degeneration
of the heart ; and it is even improbable that such affection of
the heart, apart from cerebral complications, can in any case
induce the symptom. It may be questioned whether the
rhythmic dyspnoea can be induced by reflex causes. Its occur-
rence in aortic disease (certainly its most frequent association),
as well as in aortic aneurism, would render this probable. It
is possible, however, that the aortic diseases is not causal : it
may but be the indication of arterial disease elsewhere, and the
vera causa of the phenomenon may be found in disease of the
walls of the cerebral arterioles. As a practical point, in any
case which manifests Cheyne-Stokes' respiration, you will bear
in mind the probability of disease of the vascular walls, or of
cerebral affection. I consider that the initial lesion is paresis
of the respiratory centre, and though this paresis may be pro-
duced by reflex nerve influence, it is usually a direct exhaus-
tion from cerebral causes. Once initiated, the explanation of
the phenomena on the theory of Traube is complete. In my
case the interesting fact was established that not only the
respiratory, but the cardiac centre was interfered with. The
sphygmograph gave a remarkable tracing, showing a rhyth-
mical irregularity in volume, an ample cardiac revolution being
always succeeded by one of about half its amplitude. It has
frequently been urged, that in Cheyne-Stokes' respiration the
pulse is uninfluenced, but it is obvious that in the absence of
sphygmographic evidence the observation is of little value.
In my case the peculiarity was not detected by the finger.

Having observed the general hue, posture, and
mode of breathing, you will notice whether there are
dropsical swellings of the surface of the body, pitting
with the pressure of the finger, or whether there is
evidence of fluid in the abdomen. Particularly in-
quire in what situation the cedema first manifested
itself. It is an .almost invariable rule that the dropsy,
which depends upon cardiac disease, commences at

w INSPBCTIOxV.

the feet and gradually extends over the the lower ex-
tremes. Thus it is distinguished from dropsy
dependent upon renal disease, which commences in
the face. Let me urge you, however, to receive the
evidence of patients, when interrogated as to the
locality in which the swelling first appeared, with
considerable caution. The swelling of the face mav
have been transient, and even entirely overlooked
I must reiterate the rule which J have given vn,

before— always examine the urine for albumen. If
you find albumen present, you must still proceed
with your examination of the heart, for a cardiac
complication may exist with the renal disease. If
you do not find it, you must hesitate before coming
to the conclusion that the dropsy is cardiac, for it
may be due simply to debility and anajmia. When
the patient presents the concurrence of dyspnoea on
exertion with a swelling of the feet which" pits upon
pressure, there is a strong presumption of cardiac
disease. Cardiac dropsy proceeds upwards from the
more depending parts, involving, after the legs and
thighs, the scrotum and the general areolar tissue of
the body (anasarca). The serous cavities, the peri-
toneal or the pleural, are usually the last to be af-
fected. In renal dropsy the face is generally pallid ;
in cardiac it is dusky, and the surface of the skin
is often marked by ecchymosed patches. In this
latter condition slight wounds may become serious
sores, and the sores sometimes gangrenous. The
most common cause of dropsy in heart disease is
imperfection of the valves. Of such, the most cer-
tain and most direct is disease of the valve of the
right side of the heart — the tricuspid. This disease,
however, is comparatively rare; the most common

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valvular imperfection which gives rise to dropsy is
disease of the mitral valve. Aortic lesions, however,
sometimes induce the complication. It may also
occur in fatty degeneration of the heart when there
is no valvular imperfection.

We now turn from the more general to the more
particular points of observation. Of these, first
notice the condition of the veins, especially of those
at the root of the neck— the internal jugular and the
external jugular. Notice if the veins are distended.
We have already noticed venous turgescence in the
consideration of Cyanosis, and have seen that it is a
sio-n of distension of the right side of the heart. You
observe this fulness of veins in conditions of asphyxia
— you can produce it temporarily by holding your
breath — you observe it in those who play forcibly
upon wind instruments, or in patients during the
efforts" of paroxysmal cough. In these cases there
are stasis of blood in the lung, accumulations in the
venous channels, and retention in the right cardiac
chambers. In a chronic form you may see the same
thing in patients affected with emphysema of the lung;
in these the right chambers, being in a lasting state
of distension, become dilated. Turgescence of the
superficial veins may be due, however, to valvular
lesion of the right side — to disease of the tricuspid
or the pulmonary valves. In cases of venous dis-
tension you may often note that the positions of the
valves within the vessel are marked by a slight ring
or knot ; sometimes the veins of the neck may be
seen to be varicose. Closely observe the veins to
ascertain whether they pulsate. The phenomena of
venous pulsation, though not very common, are of great
interest and importance. A very slight pulsation at

INSPECTION.

the root of the neck may be no more than natural : a
alight wave of pulsation in a more distended jugular,
synchronous with the systole of the heart, is a sign.that
the right auricle is distended, and that the contracting
ventricle communicates to it its impulse. Be careful
to note that the pulsation which appears to he in the
vein is really so. The impulse may he conveyed by
the artery beneath. To determine 'this, place your
finger on the vein and press the blood upwards for. a
short distance so as to empty a portion of the vessel ;
retain your finger thus for a short period ; then, if
there is distinct venous pulsation, you will see the
vein fill from below by jets synchronous with the
beats of the heart. In the case of arterial pulsation
beneath the vein, the latter does not fill by jets, and
you readily feel the strong pulsation of the artery.
In some cases you may observe that the pulsation is
double, at first slight, being followed by a second
stronger impulse. This is caused by the contraction
of a hypertrophied auricle communicated backwards
upon the column of blood in the vein, the closely
succeeding pulsation being due to the reflux current
impelled through the imperfectly-closed ori6ce by the
right ventricle. Venous pulse is more common and
more marked on the right side, the communication
through the innominate vein with the vena cava being
in a more direct line than obtains in the case of the
great veins of the left side. If you satisfy yourself
that there exists venous pulsation, the observation is
of high diagnostic import — it means that the tricuspid
valve is faulty, and permits regurgitation into the
right auricle.

But, perhaps, you perceive not venous, but visible
arterial pulsation. You notice, we will suppose, that

INSPECTION.

the carotids pulsate forcibly. There may be a vibra-
tion over the sternal notch due to the pulse in the aorta.
If vou look at the situation of the brachial artery in
the upper arm, along' the inner border of the biceps
muscle, you will notice a jerking movement of the
vessel attach impulse of the heart. On causing- your
patient to Hex the arm, the movement of the artery is
rendered still more pronounced. The vessel is seen to
curve outwards from the centre line of the arm with
the contraction of the heart, and then cpiickly return
to its first position. Such is the locomotive pulse de-
scribed, in association with the lesion which causes it,
by Sir D. Corrigan, and often called Corrigari 's pulse.
This phenomenon is of great importance, for it is sig-
nificant of one.of the most grave of valvular lesions;
incompetency of the semilunar valves of the aorta per-
mitting reflux of blood into the left ventricle. The
ventricle, which in these cases is hypertrophic d, con-
tracts with an exalted force and drives the jet of blood
into the arteries with a sharp and sudden stroke, but,
immediately on the subsecpient dilatation of the ven-
tricle, the arterial current flows back, leaking through
the imperfect valve, and the arteries become abnor-
mally empty. The natural result of the forcible filling
of the partially emptied tube is the jerking pulse.
You may observe visible pulsation of arteries in cases
of aneurism of hypertrophy of the left ventricle, and
especially when the vessels are tortuous and hardened
from atheroma, but this peculiar jerking pulse is
characteristic of aortic regurgitation.*

We will now narrow our area of observation to
the neighbourhood of the heart itself. First notice

* Vide subsequent Lecture on " Palpation."

INSPECTION.

whether the beating- of the heart causes vibration at
any part of the chest-wall or not. The heart-impulse
may not be visible for many causes— a thick layer of
subcutaneous fat in your patient, an encroachment
over the normal situation of the heart by a portion of
emphysematous lung, any cause which displaces the
heart from the thoracic parietes, or an enfeebled con-
dition of the heart itself. The absence of apex-beat
is only of value when taken with other signs, but it is
to be noted. Suppose that the beating'is visible in
one of the intercostal spaces, it is advisable not only
to take'a mental note of its position, but to mark it
upon the cuticular surface with a soft pencil, a
spot of ink, or tincture of iodine, or, if you wish a more
permanent record, the stain of a moistened point of
nitrate of silver.

The apex, under normal conditions, beats between
the fifth and sixth ribs. To determine the spot at which
it ought to be evident, you can make one or two obser-
vations. (1) Draw a vertical line rather more than an
inch internally to the nipple. Where this line inter-
sects, the fifth intercostal space is the spot where the
apex, in the average of healthy hearts, is evident. The
nipple can be taken as a fixed point in cases of men ;
but not so in cases of women. Then (2) draw your
vertical line two inches from the left edge of the
sternum ; where this intersects, the fifth intercostal
space is the spot required. Slight variations from this
point may be, however, not abnormal. In adult life
the apex may approach within a quarter of an inch of
the nipple-line, or may recede to two inches nearer
the sternum. I think you may take it that in adults,
an apex-beat, which is either in the nipple-line or
outside it, is abnormal. In the case of children, I

INSPECTION.

am accustomed to draw my vertical line midway
between the left edge of the sternum, and a line
dropped from the anterior border of the axilla, an apex
beat outside this line indicates an abnormality. Any
deviation, however, from the transverse line of the
fifth intercostal space is irregular or abnormal.

Many causes may produce displacement of the apex
from its normal position, but such displacement is not
usually discoverable by mere inspection. We shall,
therefore, briefly consider most of these causes here-
after. The displacement chiefly obvious to inspection
is where the apex beats below and externally to the normal
position. This indicates hypertrophy or dilatation, or
both combined, of the left ventricle. In hypertrophy
the beating- may be observed as far as the eighth in-
tercostal space, or even lower, and it is distinct, strong,
and defined. In dilatation it does not usually reach
quite so low, and is more diffused and more obvious
in the lateral direction. In hypertrophy of the right
side of the heart there is sometimes marked visible
pulsation in the space between the situation of the
normal apex and the ensiform cartilage. Note par-
ticularly the area over which the visible pulsation is
manifest. Usually it is simply a tap in the fifth inter-
space. In hypertrophy this area is enormously in-
creased, especially in children, before the ribs have
fully ossified and the cartilages have become firm. I
Lave observed the vibration in an extreme case of
cardiac hypertrophy to extend outwards as far as a
line depending from the anterior border of the axilla
downwards, to half way between ensiform cartilage
and umbilicus, and to the right to a considerable dis-
tance beyond the right border of the sternum. In
young people hypertrophy of the heart gives rise to a

INSPKOTION.

distinct prominence of the superincumbent thoracic
wall. In cases of considerable dilatation and hyper-
trophy, the movement of the chest-wall caused by the
cardiac contractions may be seen to be undulatory.
It is obvious that the motions of the muscles which
contribute to form the heart are not synchronous.
Pulsations may be seen over the situation of a dilated
auricle right or left. We shall learn in the next lec-
ture that enlarged and hypertrophied auricles can give
rise to pulsations which differ in point of time from
the ventricular contractions. This is one cause of the
apparent undulation. Adhesions of the pericardium
may increase the irregularity of the movement.

The area of visible impulse may, however, be con-
siderably increased, although there be no hyper-
trophy • in nervous palpitation, in some cases of
anaemia, in Graves' disease or in chorea, pulsation
may be observed over a space the size of the palm of
the hand. You will note, however, that in such
cases, the apex-beat is not displaced from its normal
position, nor is the chest-wall bulged outwards.

You will notice particularly whether the prfecordial
region is rendered unduly prominent. The bony
chest may be made thus prominent by rickets. You
will recognize this condition by the fact that other
portions of the thorax present nodosities, bulgings, or
irregularities. Carefully observe whether there is
any spinal curvature, for this, by causing depression
of the thorax posteriorly, may induce bulging in
front. If you are satisfied that there is distinct
prominence of the heart region you will notice
whether there is pulsation over the area — if so, you
have obtained another evidence of hypertrophy. II',
however, pulsation is feeble or absent, and the inter-

INSPECTION.

costal spaces are rendered convex, the presumption is
strong- that there is effusion into the pericardium. If
the intercostal spaces are retracted so as to be ren-
dered concave when the heart contracts, there is a
probability that pericarditis has at one time existed,
and has resulted in adhesions of the pericardium. In
some cases this retraction with the cardiac systole is
manifest in the epigastrium to the left of the ensiform
cartilage. This is due to the attachment of the base
of the° pericardium to the central tendon of the
diaphragm.

We may now recapitulate briefly the evidence
which we have obtained by inspection in relation to
its diagnostic value. We have obtained evidence
which indicates the highest point of probability in
cases of (1) cardiac malformation, producing cyanosis,
(2) Graves' disease, (3) distension of the right cavi-
ties, (4) incompetency of the auriculo-ventricular
valve of the right side (tricuspid), (5) incompetency
of the semilunar valves of the aorta, (6) hypertrophy
of the heart, (?) dilatation of the chambers of the
heart. We have gained a considerable amount of in-
formation leading to the diagnosis of (8) acute
pericarditis in cases when effusion has taken place in
sufficient amount to obviously distend the pericardium,
and of (9) a past pericarditis when pericardial adhe-
sions have taken place in any considerable degree.
We have obtained valuable evidence, though in less
degree, of (10) conjunction of renal with cardiac
disease, (11) fatty degeneration of the heart, and (12)
valvular lesions where they have given rise to
symptoms of dyspnoea.

We next propose to exercise the sense of touch to
form or confirm our diagnosis.

LECTURE III.
PALPATION.

The pulse— radial compared with cardiac— Rhythm— Effect
of effort — Position of apex-beat - Displacement— Topo-
graphy of heart— Mechanism of auricles and ventricles—
Chronometry of cardiac pulsations -Presystolic, epigastric,
and hepatic pulsation— Pericardial friction-fremitus— Thrill.

We Lave now to cause our perceptions to enter by
the tips of the fingers; we gain our knowledge
through the sense of touch.

We will first examine the pulse. It is better to do
so now that the chest, neck, and upper extremities
are exposed, in order that we may consider the radial
beats in relation with any obvious pulsations in
arteries elsewhere.

(ft.) Notice whether there be any peculiarity in the
radial artery. It may be rigid, unyielding, present-
ing irregular hard plates, as it were, embedded in
its wall. This indicates atheroma, a defeneration or
calcification of the coats of the vessel. Your patient,
in this case, will be past the prime of life, for the
condition is essentially senile. The pulse will be felt
to be hard and strong, the left ventricle having be-
come hypertrophied, and contracting forcibly to
overcome the ohstruction created by the inelastic
arteries. The changes of the radial are indicative of
like changes in many other arteries of the body.
You may probably observe the temporal artery

PALPATION.

I tortuous to the eye, and rig-id to the feel, its pulsations
visible. Frequently there is a semblance of strength
in the pulse without reality, the shock being- created
jby a feeble wave of blood in a rigid tube ; in such
jcase you will find that the impulse at the apex of the
heart is feeble ; this indicates that the atheromatous
condition of the arteries is associated with fatty de-
generation of the heart.

(b.) Observe in the next place whether there is a
I difference in volume and force between the pulsations
i of the two radials. If so, examine the brachials ; if
these are equal, the difference is merely one of ir-
regular distribution. If there is a decided difference
in the pulses of the upper extremities, there is a
probability of aneurism of one of the great vessels.

(c.) Eliminating the above conditions, we now
examine the pulse in relation to rapidity, regularity,
strength, and volume.

(1.) Notable slonmess of the pulse is generally due
rather to neurosal than to cardiac causes ; it may
occur, however, in a heart extremely weak from fatty
degeneration. It may also accompany atheroma of
the aorta, probably from mechanical irritation of the
I branches of the vagus. The pulse has been noted as
low as 20-30, and even 8-9 per minute.

(2.) Rapidity of pulse is much more common. It
I may be found associated with pyrexial conditions in
j the early stage of pericarditis, before effusion to any
amount has taken place in the sac. Very frequently,
however, abnormal quickness of pulse is not noticed
! at any stage of pericarditis. Of very far greater
j significance, is a point noticed by Dr. Walshe —
sudden variation of the rate of the pulse. In a case of
pericarditis, a very slight movement of the body may

PALPATION.

increase the pulse from 80-90 to 120-140. Unusual
quickness of the pulse occurs in many emotional
conditions, and you must not rely upon it, except in
connexion with other signs. In lesions of the mitral
valve the pulse is usually quicker than in those of the
aortic.

(3.) Force of the pulse.— -This is a point of great
moment, The apparent force of the pulse is notably
increased in two conditions— hypertrophy of the heart
and regurgitation through the aortic valves. It is
diminished in degeneration of the muscular fibre of the
heart, in dilatation of the cavities, and in most of the
valvular affections.

In hypertrophy we find the pulse strong, full, and
incompressible. As you feel the radial pulse with
one hand, place the other upon the thorax over the
heart-region, and you will find a strong, heaving,
prolonged cardiac impulse as an accompaniment.
There is an expression of power, both about pulse
and apex-beat, which is quite wanting in simply
functional excitement of the heart. In the latter
case the stroke is not sustained, but abrupt and
brief.

The other cause of exalted force of pulse, aortic
regurgitation, has already been indicated to us by
signs which we have considered under " Inspection."
The pulse is first jerking, then collapsing ; the artery
strikes rhe finger with a sudden blow.

Suppose now that, on the other hand, you find the
pulse small and feeble, it is a good rule to elevate the
patient's arm vertically above his head, and observe the
characters of the pulse in this position. This will enable
you to eliminate doubtful cases of aortic regurgitation
in which the pulse has become temporarily feeble ;

PALPATION.

in the aortic regurgitant lesion the pulse will become
-intensified instead of enfeebled, its hammer-like cha-
racter exalted, and the patient may complain of dis-
comfort. In most of the other valvular lesions, aortic
obstructive disease excepted, in which no influence
probably will be detected, the pulse is enfeebled by
the vertical position of the arm. In some cases of
mitral disease, and in conditions wherein the heart-
muscle is feeble, the radial pulse in this position
may be quite extinguished. The same occurs, how-
ever, equally in anaemia. The pulse being per-
ceptible, notice whether the vertical position in-
duces irregularity, especially irregularity of volume.
If so, there is a probability of disease of the mitral
valve.

You snould now, while still keeping the finger
upon the radial pulse, examine with your other hand
the situation of the heart's impulse. It is very im-
portant if you note that, though the heart's con-
traction is strong, the pulse at the wrist is small and
weak. This suggests imperfection of the mitral
valve, inducing either regurgitation or obstruction.
In mitral regurgitation the current of blood which
should, by the contraction of the ventricle, be forced
into the aorta, and thence to the systemic arteries, is,
by the leak in the mitral valve, in part diverted to
the left auricle. The pulse, therefore, is not pro-
portionate to the strength of the heart's contraction,
but is enfeebled in ratio to the amount of blood lost to
the arteries by regurgitation. In mitral obstruction,
the pulse is weak because the blood reaches the left
ventricle with difficulty, and the latter contracts on
an insufficient amount. It is not often possible by
mere observation of the pulse to differentiate between

PALPATION.

obstructive and regurgitant lesions at the mitral
orifice. The irregularity so often attributed to the
pulse of mitral regurgitation I consider to indicate
engorgement or dilatation of the right chambers
of the heart. For arguments see Part II. In
many cases of mitral regurgitation the pulse appears
to be quite normal. This indicates either that only a
small quantity of blood is lost to the systemic arteries
by such regurgitation, or else that the left ventricle
has become hypertrophied sufficiently, and contracts
with adequate force, to compensate for the obstruc-
tion caused by the reflux into the auricle. If you:
notice the pulse to be persistently weak, the contrac-
tions of the heart feeble, and yet by examination you
find no evidence of valvular disease, there is a strong
probability that the heart-muscle is enfeebled by
degeneration.

If you find that the pulse is feeble, although the
hand, placed over the preecordium, detects tolerably
strong pulsation, and yet evidence of valvular disease
is absent, then it is very probable that the hyper- j
trophy of the heart causing the strength of systole is
in the right ventricle, and not in the left.

In all cases in -which there is a morbid condition of tile
right chambers of the heart, the radial pulse tends to be weak.
The supply to the left ventricle is from the lungs; if, from
any defect in the right heart, the lungs are ill supplied with
blood, the left ventricle is also insufficiently supplied, and
thus the systemic arteries are imperfectly filled.

Occasionally you may find that the hand on the
precordial region is sensible of a contraction, which
does not make itself evident by a pulse at the wrist —
there is an ineffectual systole. The ventricular con-
traction is at such times too feeble to produce a sen-

PALPATION. 00

sible pulse in the remote arteries. It may be found,
.however, that, though lost in the radial, the pulsation
can he detected in the larger arteries nearer the heart,
such as the carotids. This is but a less significant
expression of the conditions we are about to consider
— viz., irregularity and inter mittcncy.

(4.) Rhythm of the pulse.— Carefully distinguish
I between irregularity of volume and irregularity in tine.
i In the former case the pulse is felt to occur at equal
intervals, but is fuller at one beat than at another.
You are sensible that varying volumes of blood are
transmitted by the various contractions of the ven-
tricle. This condition is rendered more evident by
elevation of the arm, and the observation may give
you an important aid to diagnosis. It is almost
pathognomonic of mitral regurgitation with yielding
of the right chambers.

We will- suppose that the pulsations are irregular
in time. Irregularity and intermittency are condi-
tions which differ only in degree, so we will here con-
sider them together. In intermittency, the pause
between the pulses is longer, there being an interval
equal to that occupied by a pulsation. The first
thing I have to urge upon you is to be very careful
in giving this phenomenon its due weight in a dia-
gnostic sense, and nomore. I am afraid that mischief
has been done many times by a hasty opinion to the
effect that a patient has heart-mischief, when this
sign has been too exclusively relied on. Remember
that irregularity or intermittency of heart's action,
and consequently of pulse, may coincide with organic
integrity of heart, and even with good health. The
first question I would ask you to propound to your-
selves is : — Does this irregularity co-exist with a fair

°* PALPATION.

strength of impulse, as felt over the pracordium or
otherwise ?

Iptermittency maybe merely a constitutional pecu-
liarity. It may be due, as Dr! B. W. Richardson has
shown, to causes operating- upon the general nervous
system. It may be superinduced by strong emotions,
by terror, anxiety, grief, pain, fatigue ; it may occur
in organic diseases of the brain. It may be tem-
porarily caused by attacks of indigestion. In the
absence, therefore, of a notable feebleness of heart-
beat, and excluding other diagnostic signs, you are
not to conclude from mere intermission of heart and
pulse that organic cardiac disease exists.

If, however, notable feebleness of impulse co-exists
with irregularity, and especially ineffectual systole, it
is of serious diagnostic import. It is the sign, the
very early sign it may be, of a strike on the part of
the left ventricle. Too languid to contract from the
ordinary stimulus of the blood with which the
auricle by its single contraction supplies it, it waits
until a second, or even a third, contraction of the
auricle has supplied it with more. This is the condi-
tion which obtains in mitral regurgitation and in '
dilatation of the ventricle. It is pathognomonic of
dilatation of the left ventricle, and indicates that the
muscular fibres have become degenerated, and have
lost their tonicity. Most commonly it is associated
with mitral regurgitation, which is the frequent in-
ducing cause of such dilatation. When you observe
in a case of mitral disease that the heart's action
assumes this character, note it as a sign of prognostic
import. In the absence of signs of valvular disease,
the observation is of importance, both from a dia-
gnostic and a prognostic point of view. When you

PALPATION.

find it in conjunction with senile changes— with
feeble but diffused impulse, with atheromatous vessels,
f arcus senilis " of cornea, &c, you may know that
a heart at one time hypertrophied has become de-
generated, that it will never recover its power, and
that the patient trembles on the verge of life.

A further question I would ask you to propound
to yourselves when you notice in any patient irregu-
larity or intermittency of heart's action is : — What is
the effect of effort upon this heart ?

An irregularity which is merely neurosal is scarcely
affected by effort ; the pulse is quickened of course,
but its irregularity is often diminished rather than
increased. When the irregularity is clue to cardiac
imperfection, however, very slight effort, such as
making your patient walk briskly for a minute or
two up and down the room, notably increases such
irregularity. When there is dilatation, palpitation
usually precedes the more pronounced irregularity ;
but when degeneration has proceeded far, the halting
action takes place without notable quickening.

Notice also whether effort on the part of your
patient causes distress, and what is the form of such
distress. Little or no discomfort occurs in neurosal
irregularity. In dilatation you find palpitation and
dyspnoea ; in degeneration, faintness and dyspnoea ;
in certain rare cases the ventricular halt is accom-
panied by horrible sensations, and a fear of impending
death. Such was noticed by Romberg in a case in
which a tumour involved the va^us nerve.

We turn from the consideration of the pulse* to that
of the cardiac area itself.

* For further particulars as to the signs afforded by the
pulse, see Part II.

PALPATION.

We have noted in our inspection of the chest
where the impulse of the apex of the heart should be
manifest. We proceed to confirm or enlarge our
observation by placing the hand over this region.
Suppose that

(a.) The apex-beat is feeble or indistinguishable. Be-
fore recording- this as a positive observation, let your
patient sit up and lean well forward ; an apex-beat
may then become evident which was before unde-
tected. If notable feebleness of the beat be associated
with weakness of the pulse and the signs we have
before recorded as pertaining to the affection, you
have gone very far towards the diagnosis of fatty de-
generation of the heart. In rare instances, such
feebleness may be found to be due to pericardial
effusion ■ in such case the postural change just noted
will serve you in good stead as an additional means of
diagnosis, for the tilting forwards of the body may
render evident the apex pulsation in a situation above
the normal, probably in the fourth intercostal space,
the fluid in the pericardium having tilted the apex
upwards to this level. Palpation is of high im-
portance in thediagnosis of pericarditis with effusion.
In the earlier stages of the affection yon may find
excited, diffused, and, sometimes, tumultuous action
of the heart with the general signs of pyrexia; as
effusion takes place the apex-beat is enfeebled and
carried upwards and to the left of its normal posi-
tion ; then, if distension be extreme, the beat is no
longer to be felt. You must, however, draw no hasty
conclusion from the observation that the apex-beat is
feeble or imperceptible to the touch. It may be thus
because the heart is overlapped by emphysematous
lung, or on account of a thick layer of subcutaneous

PALPATION.

fat in your patient, or, even in health, in persons with
deep chests. You may readily understand that m
women with full breasts the apex-heat may not he
perceptible to the touch. It is a fundamental rule,
however, that you should always observe in cardiac
diagnosis— to fix the exact spot of the apex-beat. If in-
spection and palpation fail to do this, you will
proceed to determine it by auscultation, as we shall
hereafter consider.

We will now suppose that you have been able to
feel the apex-beat, and have compared its position with
that which it should normally occupy, as we have
determined in the Lecture on Inspection. You will
find that

(b.) The apex-heat is displaced from its normal position.
Such displacement may take place from disease of the
neighbouring- textures and organs. Pleuritic effusion
in the left cavity of the thorax may push the heart
completely to the right side, so that the impulse which
is wanting- on the left side is felt right of the sternum ;
effusion in the right thoracic cavity, on the other hand,
may push the apex left of its normal position. Em-
physema of the lung; pushes the heart downwards and
towards the epigastrium, and oftentimes in this disease
you find an impulse below the ensiform cartilage ;
you must examine further, however, before concluding
that this is the apex-beat, for in emphysema the right
side of the heart is usually enlarged, and the impulse
which you feel is caused by the contraction of the
right ventricle, the tip of the left ventricle being out-
side the point of obvious pulsation. Another disease
of the lung which may give rise to a singular displace-
ment of the apex-beat is fibroid phthisis ; in such
condition, when it affects the left lung, you may find

° PALPATION.

the chest-wall drawn inwards and the heart so dis-
placed that its apex heats at or above the fourth rib
lumours, aneurism, or cancer occupying- the thoracic
cayity may also cause displacement of the heart •
enlargement of the left lobe of the liver, cysts, abdomi-
nal tumours, and dropsy, may produce a like result.
We have already said that pericardial effusion tilts the
apex upwards. All these causes must be eliminated
by careful examination.

In the rare cases of transposition of the viscera, the apex of
the heart is found to beat under the right, instead of under the
left nipple. The liver dulness then occurs on the left, and not
on the right, side, whilst the stomach is to be recognized on the
right.

We come now to causes of displacement intrinsic to
the heart itself.

When the heart-apex is found to beat below and to
the left of its normal position (fifth interspace and
two inches from left border of sternum, or about an
inch right of a vertical line through the nipple),
you may diagnose hypertrophy of the muscular wall
of the left ventricle or dilatation of the ventricular
cavity. The sensations communicated to your fingers
aid you to differentiate those two conditions. Remem-
ber that hypertrophy means power, and dilatation weak-
ness, but the phenomena and their causes may be
variously combined. A full, long, and heaving stroke
is characteristic of hypertrophy ; an excited, short,
diffused, struggling beat indicates dilatation. Action
with power is shown in the one case, excitement with-
out power in the other. In hypertrophy and dilatation,
the apex may be felt two or three inches, or even
more, outside the nipple-line, and as low as the
seventh or eighth intercostal space. If the apex
happen to beat against a rib the shock is, of course,

PALPATION.

subdued ; it is necessary to recollect this, otherwise
you might put down as feeble, an impulse which is
really strong.

We now consider not only the situation of the tactile
pulsation, but the extent of area over which it is mani-
fest. Normally, as I have said, only a tap in the fifth
interspace is felt ; pulsation may be evident, however,
over a superficial inch in strictly normal conditions.
Pulsations in other positions may possibly be evident
in health. Such may be felt in slight degree in the
| fourth intercostal space ; or, and this more commonly,
in the epigastrium to the left of the ensiform cartilage.
By pushing the fingers upwards beneath the false ribs
on the left side, you may sometimes feel the throb of
the right ventricle. You must give these contingencies
due weight, but, as a general rule, any pulsation
manifest in other situations than the neighbourhood
of the normal apex, is evidence of disease of the heart
or the great vessels. We proceed to consider the
conditions wherein

(c.) Pulsations, apart from the apex-beat, are mani-
fested over the cardiac area. To appreciate these we
should endeavour to obtain an idea of the normal
Topography of the Heart. The area occupied by
the healthy heart may be thus roughly illustrated on
the thoracic wall :— Draw a line, a little externally to
the right border of the sternum from the second inter-
costal space to a point just below the fifth sterno-costal
articulation. Draw a second line from a point just
below the second sterno-costal articulation on the left
side to the situation of the normal apex. Unite the
extremities of these lines respectively above and below,
so as to describe a quadrilateral figure. Of this super-
ficies (which will be bounded above by the aorta which

PALPATION.

crosses from right to left, and below by the diaphragm)
about four-fifths are occupied by the right ventricle,
which lies immediately behind the sternum and the
third, fourth, and fifth costal cartilages of the left
side, and culminates in the pulmonary artery at the
second (left) interspace close to the sternum. The
left ventricle is chiefly posterior ; but it borders the
right ventricle to the left from the third sterno-costal
articulation to the apex, which itself constitutes. The
right auricle is in the third interspace (right) and
behind the third and fourth cartilages. The left
auricle is for the most part overlapped by the pul-
monary artery, but a small part of it is situated
superficially in the second interspace left of the
sternum.

If you find a forcible impulse of the heart towards
the left of the border we have sketched as the normal
left boundary of the cardiac area, the apex strongly
defined in its beat and manifest below and to the left
of its usual place, the pulse being full and strong, you
may conclude that there is hypertrophy of the lejt4
ventricle. If you find a strong impulse in the epigas-
trium extending from the normal apex to the right of
the ensiform cartilage and sternum, and yet a much
weaker pulse than you would think such a systole
would produce, you probably have hypertrophy of the
right ventricle. Tuck your fingers under the false
ribs to the left of the ensiform cartilage, and you will
feel the contraction of the ventricular wall. We shall
return hereafter to epigastric pulsations.

As I have before said, hypertrophy and dilatation
are often combined. When the left ventricle is
dilated as well as hypertrophied, palpation gives you
a less localized and less firm and strong impression.

PALPATION.

The impulse is more diffuse, the apex feels less
pointed, and more rounded or globular to the finger.

When the left ventricle is dilated, hut not hyper-
trophied, you feel its impulse over a wide area in the
situation indicated, but it is felt as a short excited
" slap."

Hypertrophy of the rig-ht ventricle scarcely ever
exists without dilatation.

It has been supposed that auricular hypertrophy is
not to be demonstrated by physical signs. I shall
presently show you that this is not the case, for I
have in many instances been able to demonstrate
upon the surface of the chest-wall the contraction
both of the right and of the left auricle.

When you have a general dilatation, or hypertrophy
and dilatation combined, of all the cavities of the
heart, the hand and the eye both perceive a fluctua-
tion— or, as Dr. Walshe has expressed it, a seeming
undulation — over the extended area over which the
contractions of the cardiac chambers are manifest.
This is obviously clue to the fact that the contractions
of the muscular walls of the various chambers are
occurring not simultaneously, but in successive
moments of time.

We will briefly consider the mechanism of the
muscular walls of* the heart. We should remember
that the auricles and ventricles possess the double
function of reservoirs and propellers. Such function is
exercised in alternation — at rest they are reservoirs,
in action they are propellers. You know that the
rhythm of the heart comprises a period of contraction
(systole), and a period of rest and dilatation (diastole).
The latter occupies much the longer time : as a rule,
the systole occupies one-fifth of the period ; the

VmJ PALPATION.

diastole, of course, the remaining- four-fifths. During-
the period of repose, what is taking- place ? On the
right side of the heart, the great veins of the body,
the superior vena cava, and the inferior vena cava, are
pouring- their impure venous blood into the right
auricle, which is gradually filling- ; the ventricle" is
becoming- filled at the same time, for, the auriculo-
ventricular valves being- now flaccid, auricle and ven-
tricle form oue cavity. On the left side of the heart,
the pulmonary veins are carrying- the pure blood,
which has been aerated in the lungs, to the left
auricle, and hence to the ventricle, these cavities
becoming- filled simultaneously with the right.
During- all this period, the muscle of auricles and
ventricles is receiving- its nutrient supply, for the
heart differs from all the other structures of the body
in that, whilst the latter are supplied with blood by
the heart's contraction, itself receives its arterial
supply during- its own period of repose. The muscle
of the heart is supplied with blood through the
coronary arteries, which arise from the aorta (pouches
of Valsalva) just above the semi-lunar valve*. The
open mouths of these arteries had just been occluded
by the flaps of the valves whilst the aortic orifice was
open, but now in diastole, the valves falling- back
from the weight of the superincumbent column of
blood and closing- the aortic aperture, the channels
are opened for the sudden in-rush of the stream of
arterial blood into the tissue of the heart.

The cavities having- become replete, the contraction
of the heart, the s}rstole, begins. The important point
to notice is, that this contraction is not synchronous
throughouut all the muscular cavities of the heart ;
but that the auricles always contract before the ventricles.

PALPATION.

You are aware that the fibres which constitute the
muscle of the heart are under the control of the
minute ganglia of the sympathetic nerve ; the action
of these ganglia is, however, controlled and co-ordi-
nated by the vagus nerve, which restrains contraction
until the movement shall be uniform and regular.
The necessary stimulus to the contraction of the
auricle is distension ; until it is sufficiently filled with
hlood, its systole does not occur. Distension, then,
provokes auricular contraction, and the ventricle
which has already been filling- by the passive flow of
blood into it, is now more completely gorged by the
additional blood forced into it by the auricle. In the
normal heart, this precedence in action of the auricle
is only momentary, the wave of contraction speedily
ensuing- in the ventricle. Still, it is of hig-h impor-
tance to realize this priority of auricular contraction.
Thoug-h the arrangement of the muscular fibres of the
heart is such, that many of the fibres are common to
all the cavities, yet the auricles are much more inde-
pendent of the ventricles than the ventricles are of
each other. Extremely early in foetal life there is a
mark of differentiation of the then sing-le auricle
from the single ventricle, but the fight ventricle is
formed by a doubling- over of a part of the original
(left) ventricle.

The necessary stimulus, then, for the contraction
of the ventricles, is the extra repletion induced by
the immediately preceding contraction of the auricles.
The ventricular contraction, though strictly speaking
vermicular, occurs in such a brief moment of time, that
it is indistinguishable save as one movement in syn-
chronism. The simultaneous contraction of the ven-
tricles driving the blood into the aorta on the one

PALPATION.

side, and the pulmonary artery on the other, the apex-
beat, the pulse in the aorta, and the pulse in the pul-
monary artery, are practically coincident in time.

I have said that in the normal state of the heart
the pulsation of the auricles causes no apparent vibra-
tion of the thoracic wall ; it is not so in disease, how-
ever ; hypertrophy and dilatation of right or of left
auricle may give rise to a visible pulse. As regards
the right auricle, this has been generally admitted.
The right side of the heart becomes dilated, and often
hypertrophied, under all the circumstances which
induce an undue repletion of the venous system. We
have already alluded to these conditions, and we shall
again briefly consider them in the next lecture. The
right auricle is never hypertrophied and dilated with-
out the right ventricle being in like condition. Under
such circumstances you feel a heaving impulse, which
seems to be very near the surface, extending from the
normal apex across the epigastrium to the right side
of the sternum ; this is caused by the right ventricle,
and. you may feel a pulsation in the second or third
intercostal space just right of the sternum, which is
caused by the auricle. How to determine this we shall
presently consider.

We turn to the left auricle. Undoubtedly, in certain
cases, you may observe a pulsation in the second, third,
or fourth intercostal space left of the sternum, but is
this caused by the auricle ? On this point there has
been difference of opinion. Some writers have stated
that inasmuch as the greater part of the auricle is
covered by the great arteries emerging from the heart,
and the muscular walls of the auricle are comparatively
thin and feeble, its power of contracting with sufficient
force to produce an impulse is improbable. These

PALPATION. vo

observations are undoubtedly correct in reference to
the left auricle when in a state of health. It is a very
different matter, however, when it is m a state ot
disease. There is one condition of disease or malforma-
tion, which gives rise to great hypertrophy and dilata-
tion of the left auricle— narrowing (stenosis) of the
auriculo-ventrimdar orifice of the left side (mitral). The
causation of this hypertrophy and dilatation is easy to
understand. I have explained that the contraction ot
the auricles is necessary to produce that perfect reple-
tion (that additional supply to the already partially
filled ventricle) which is required to call forth the
ventricular systole. When the aperture between
auricle and ventricle is so narrowed as to become an
obstruction, the auricle has perforce to contract with
enhanced power to overcome it. The auricle thus
called upon for abnormal force of contraction becomes
hypertrophied, and, from being in a state of preter-
natural distension, dilated. In the case of a boy of
nine, who had constriction of the mitral orifice, I
found at the post-mortem examination that the mus-
cular wall of the left auricle was from \ to \ inch in
thickness* The normal thickness of the left auricle
in adult life is somewhat more than TV inch.f Ac-
cording to Bouillaud, it is & i^li. Here was an
auricle, the thickness of the muscular wall of which
was in great part, thicker than the thickest part of the
normal adult right ventricle. Who could doubt the
ability of such an auricle to communicate a distinct
pulsation to the thoracic wall ?

The foregoing considerations will point us to a plan

* Medical Times and Gazette, January 10, 1874, p. 35.
t Flint, "Diseases of the Heart," 2nd edition*, p. 21.

PALPATION.

,lemonstratiilfi- such puisations as are cauged . the
auricles. A pulsation left of the sternum may be due
to the contraction of the left ventricle, the pulse in
the pulmonary artery, or the contraction of the auricle.

Pulsation right of the sternum may be due to the
contraction of the right ventricle or the right auricle,
to the pulse in the aorta, or some aneurismal dilata-
tion ol that vessel. To determine whether the pulsa-
tions are, or are not auricular, we may adopt a simple

plan Of CHRONOMETRY OF PULSATIONS OCCURRING

over the cardiac area. It has been recommended
that the movements of two doubtful points of pulsa-
tion should be compared by attaching- to each, by
means of a pellet of beeswax, a bristle carrying a
small paper flag-. The variation in time of the two
movements is observed by the vibrations of the flag.
The modification of this valuable plan which I adopt,
is the following :— Cut two small circles of sticking-
plaster, about the size of fourpenny-pieces ; transfix
the centre of each by a pin, so that the head is in
contact with the adhesive side of the plaster. Attach
the one adhesive circle over the site of pulsation sup-
posed to be auricular, aud the other over the situation
of the apex of the heart. The shafts and points of
the pins projecting forwards, you have two levers
which vibrate with the movements communicated to
them by the several pulsations; these levers you
elongate by attaching to them rolled " spills" of tissue
paper. A still simpler plan, which I now generally
adopt, is to pull out a small piece of cotton wool into
the form of a tall cone and attach it by its base to the
pulsating portion of chest-wall by means of a little
ointment. Any number of these can be applied
over points of pulsation, and the relation of their
vibrations be thus compared.

PALPATION.

If vou have to do with an auricular pulsation you
•will see that the movement of its lever mvanably
precedes that of the lever adapted over the hear
aoex The movement is presystolic, and must be due
to the contraction of the auricle. If the two con-
tractions occur simultaneously they must be produced
by the ventricle or in the pulmonary artery or aorta.

Pulsation of the pulmonary artery which may be
felt between the second and third ribs, close to the
left border of the sternum, is only manifest when
from any cause the left lung is retracted from the
base of the heart. You feel that such iff™*
verv superficial ; it is said that even the click of the
pulmonary semilunar valves may be felt as a li : le
shock to the finger. It is interesting- to note the
relation of this phenomenon to respiration. It the
luno- be only partially retracted from the pulmonary
artery you will observe the pulsation to become more
and more visible during- expiration, whereas, during-
inspiration, as the l.mgs, becoming more and more filled
with air, encroach over the heart, the pulsation becomes
less and less evident till it ceases, reappearing at the
next inspiration.

Pulsations of the aorta, which, of course, occur on
the ooposite-the right-side of the sternum, may be
due to aneurism, or to displacement of the vessel which
occasionally occurs in rickety chests.

It remains for us to consider pulsation felt at the epigas-
trium. We have already noticed the pulsation due to
adisplaced or hypertrophied and dilated right ventricle.
Any considerable enlargement of the right side of the
heart will give rise to a pulsation felt at the epigas-
trium. An impulse is sometimes communicated to the
edge of the left lobe of the liver, which is to be felt

PALPATION.

below the ensiform cartilage. Occasionally, but very
rarely, the impulse is reversed; the integuments at the
epigastrium are felt to be retracted, instead of propelled
at each systole of the heart. In such cases there has
been an extensive pericarditis, which has resulted in
adhesion of the heart to the diaphragm and the liver.

But we have to consider pulsations felt at the epigas-
trium, which may be due to other causes, with a view
to differential diagnosis. We will suppose that :

{A.) The pulsation is felt in the median line, that is,
the line joining the ensiform cartilage and the umbili-
cus. It will probably occur to you that such pulsation
may be due to aneurism of the abdominal aorta. The
suggestion readily occurs, but though you feel a for-
cible pulsation over the vessel, you must hesitate very
considerably before committing yourself to the opinion
that it is due to an aneurism. Abdominal aneurism is
rare. " So," as Sir William Jenner has said, " instead
of being your first, it should be your last idea, that an
abdominal pulsation is due to aneurism."* If there be
an aneurism, you will feel a localized swelling of the
vessel, which with, or just after, the systole of the
heart expands ecpially in all directions, above, below,
and laterally. A tumour, superficial to the aorta, may
pulsate from the communicated impulse of the vessel ;
but then you will feel no lateral pulsation. You may
find assistance in the diagnosis, by causing your patient
to bend forward on the hands and knees ; a tumour
isolated from the vessel then recedes from it, and you
no longer feel the pulsation, which in aneurism is
unaffected by this position. Having eliminated abdo-

* Clinical Lecture on Tumours of Abdomen : British Medical
Journal, 1869, p. 42.

PALPATION. 6^

minal aneurism and tumours to which the ahdominal
aorta may communicate its impulse, we will suppose
that you yet find a pulsation in the central line, below
the ensiform cartilage, which you have convinced your-
self by palpation under the false ribs, is not clue to the
impulse of the right ventricle. You will find such a
pulsation very commonly ; it is the pulse of the abdo-
minal aorta. In the vast majority of abdominal pul-
sations there is no structural alteration to account for
them ; they are palpitations due to neurotic conditions.
The abdominal aorta shows the excited pulse that the
other great arteries of the body manifest. This pheno-
menon is, of course, most evident in spare people ; you
will find it in cases of anaemia, in dyspepsia, and spe-
cially the dyspepsia of old people whose arteries have
commenced to degenerate. We will consider in the
nest place that :

(B.) The pulsation is felt to the right of the median
line. I have said that the beating ventricle may propel
the edge of the left lobe of the liver ; an aneurism may
do filename still more extensively ; but in some cases
it may be observed that the whole liver pulsates. This
phenomenon is of rare occurrence, but it is of great dia-
gnostic importance : it indicates regurgitation through
the tricuspid orifice. The liver, in this condition, is
like an erectile tumour ; it pulsates with the systole
of the heart. The right ventricle, by its contraction,
instead of driving all the blood it contains into the
pulmonary artery, on account of the imperfection of
the tricuspid valve, forces some of its contents back
ao-ain into the right auricle. Consequently, an impulse
is given to the blood contained in the vessels opening
into the auricle— i.e., the great systemic veins and
their tributaries. Hence the rhythmical injection of

PALPATION.

the hepatic veins, and the consequent pulsation of the
liver.* You will see that this phenomenon is exactly
analogous to the venous pulse in the jugulars which
we have before noticed. Both indicate the same
morbid condition of the heart, tricuspid insufficiency.
Suppose, now, that :

(C.) The pulsation is felt to the left of the median line.
This may be due to an aneurism of the abdominal aorta,
especially when it involves also the superior mesen-
teric artery. I once met with a case in which there
was pulsation felt to the left of the middle line, midway
between ensiform cartilage and umbilicus. The pul-
sation gave rise to distress, and was associated with a
fulness at the epigastrium. The case had been diag-
nosed as one of cancer of the liver. Whilst, however,
it was evident that the left edge of the liver encroached
over the epigastrium, I could find no signs leading to
the conclusion that there was any malignant disease.
The left side pulsation was very difficult of explanation.
I had the opportunity, however, of seeing the case
several times, and I found (1) that the pulsation always
became pronounced just previously to the cata-
menial period (the patient, a woman of full habit, was
nearing the climacteric), and that it diminished almost
to extinction, after the period was passed; (2) that it
was always controlled, even to almost extinction, by
large doses of quinine. The view that I took of the
case was, that the pulsation was in the splenic artery.
The patient completely recovered.

"We have hitherto considered the evidence afforded
by the well-known phenomenon, pdsation, as detected

* Aided perhaps by the pulsation of the inferior cava which
lies behind the liver.

PALPATION.

over the cardiac area. Now we have to consider other
peculiar diagnostic signs recognizable to the touch.

The Special tactile phenomena manifest
over the cardiac region are briefly, («) friction,
(*) thrill.

(a.) On placing the hand over the prfecordium, you
may, in certain cases, detect a sensation of rubbing
accompanying the systole and diastole of the Jieart.
You should cause the patient to hold his breath so as
to convince yourself that the sensation is not com-
municated by any part of the respiratory mechanism.
If you feel that the periods of contraction and dilata-
tion of the heart are accompanied by this feeling of
friction, you may be sure that your patient is suffering
from pericarditis. The phenomenon is termed peri-
cardial friction-fremitus; itis not common; in a very large
proportion of cases of pericarditis it is not observed.
There must be the concurrence of certain conditions
to produce it. The pericarditis must be in an early
stage ; it occurs only at the commencement of effusion
into the pericardial sac : the fluid effused must be
thick or rich in fibrine ; at autopsies in some cases of
pericarditis, you may see the surface of the heart
covered by a layer of material like soft butter, this is^
the kind of effusion which gives rise to the feeling of
friction : the amount of fluid must be limited ; as the
pericardial sac becomes distended the exudation is less
viscid, the heart is separated from the thoracic wall,
and the systole is enfeebled — all these causes concur
to prevent the sensation of pericardial fremitus : lastly,
the heart must contract with sufficient force ; a feeble
heart does not produce it. This sign never occurs
without the friction being recognizable by the ear, as
we shall hereafter describe. You will find a great

PALPATION.

number of cases of pericarditis occurring without this
sign, but, where you observe it, it is of great import-
ance ; for it renders certain the diagnosis of pericar-
ditis, and it enables you to state that the pericardial
surfaces are roughened, or that the effused material
is of a viscid character.

We come now to an interesting phenomenon, which
will well repay careful investigation. This is :

(b.) Thrill. On placing the hand over the praecor-
dium you are sensible of a peculiar vibration occurring
over a certain area and at a certain period of the heart's
action. The vibration is quite characteristic ; a sense
of trembling is communicated to the fingers— rapidly
as if the finger touched the twanged string of a violin
or comparatively slowly as if the vibration had pro-
ceeded from the bass string of a violoncello. The
French observers aptly compared the sensation to
that experienced when one places the hand on the
back of a purring cat or kitten ; they gave to the
phenomenon the name of fremissement cataire. It is
characterized also by the terms purring tremor, and in
German, Eatzenschnurren. It is not sufficient, how-
ever, merely to note the existence of this sign.' You
must especially establish, (1) its position" (2) its
rhythm.

You may feel it over the base of the heart, about
the second intercostal space and right of the sternal
border. Placing the tips of the fingers over the
situation where the thrill is felt, now touch with the
fingers of your other hand the spot where the heart's •
apex beats. This will enable you to determine the
rhythm of the thrill. You find, we will say, that the
thrill coincides in time with the apex-beat. Then you
have either contraction (stenosis) of the aortic orifice

PALPATION.

„ aortic aneurism. You will notice whether the latter
condition is indicated by a pulsatile swelling or the
concurrent signs of aneurismal dilatation of the aorta.
If not, you will proceed to confirm your diagnosis of
aortic stenosis by auscultation and the means we shall
hereafter describe. In rare cases the purring tremor
may be felt over the situation of the pulmonary artery;
it indicates obstruction of that vessel. Perhaps, how-
' ever, you find that the thrill does not coincide with
the beat of the apex but occurs during the diastole of
the heart. A diastolic thrill is rare ; it is character-
istic of regurgitation through the aortic orifice. It
signifies that the aortic valves cannot perfectly close,
that they permit reflux of blood. So you may find
this sign in conjunction with the phenomena we have
noted as occurring in a like condition — forcible apex-
beat and locomotive (Corrigan's) or water-hammer
pulse.

Suppose, however, that you feel a thrill at or near
the apex of the heart. In this position it is of the
utmost importance to establish the rhythm of the
thrill. I always advise that for this purpose you
employ the fingers of each hand, as in the case of
aortic thrill. First determine the spot at which the
apex beats. You may find that this is also the point
of greatest intensity of the thrill ; to assure yourself
of this, however, place a finger of your other hand a
little externally. You will then convince yourself
whether thrill and impulse occur together ; in other
words, whether the thrill is systolic. If so, if thrill=
impulse, it is caused by regurgitation through the
mitral orifice. Such a thrill is not common. You
may find, however, and much more commonly, that
the thrill felt in the neighbourhood of the apex

'* PALPATION.

is not exactly simultaneous with the systole. You
distinctly recognize that the finger which receives
the impression of the thrill does so just before the
finger of the other hand receives the impression of the
impulse of the ventricle. The thrill is abruptly ter-
minated by the ventricular systole— it is presystolic.
Moreover, you may find that it is felt not just at the
apex, but slightly internal to it, and at a higher level.
This separation of thrill from apex-beat renders the
detection of the rhythm of the former more easy by
the rule which I have laid down. Always investigate
the phenomenon of thrill by using both hands, examining
the site of the thrill by the. finger or fingers of the one hand,
and noting the apex-beat by the finger or fingers of the other.
It will be found that of thrills about the apex, that
which is presystolic in rhythm is by far the more
common. To recognize it is of very great importance.
It is pathognomonic of contraction (stenosis) of the
mitral orifice, and is due to the vibration caused by
the forcible contraction of the auricle urgiiig the blood
through the obstructed outlet into the ventricle. We
shall return to this subject when we come to auscul-
tation, and consider the relation of thrill to murmur,
but it is necessary to premise that both thrill and
murmur are due to a like cause, but that we may have
thrill without murmur and murmur without thrill.
Vibration produces both phenomena ; if the vibrations
be insufficiently rapid they cannot be perceived by the
ear, whilst they are obvious to touch ; again, they
may be so rapid as to be undetected by touch but
detected by the ear ; or the material which conducts
the vibrations may be more suitable to convey impres-
sions of touch in the one case, and of sound in the
other. I wish strongly to insist that you shall give

7f»

PALPATION.

due prominence to investigation by the sense of touch,
and not fell into the error of esteeming auscultation
the be-all and end-all of cardiac diagnosis. I have
had cases in which the existence of thrill, presystolic
in rhythm, led me to the diagnpsis of mitral stenosis,
thouoh, in the one case, there was no murmur at all,
and in the other it was so short as to be scarcely dis-
tinguishable. You must by no means draw any con-
clusion from the absence of thrill, but where you find
a well-marked thrill hefore the impulse, you have, m
my opinion, a certain sign of constriction of the mitral
orifice.

We may thus summarize the diagnostic evidence to
be obtained from the purring tremor. Felt over (a)
the base of the heart its rhythm may be (1) systolic
or (2) diastolic. If (1) systolic, it indicates (exclu-
ding aneurismal thrills, which are outside oiir subject,
and°the rare thrill denoting obstruction of the pul-
monary artery) a morbid condition of the aortic
valves which has resulted in a narrowing of the outlet
from the ventricle. If (2) diastolic, it indicates
regurgitation into the left ventricle, owing to imper-
fect aortic valves. Felt over (ft) the apex of the heart,
the thrill may be (1) systolic, or (2) presystolic*
Systolic thrill indicates regurgitation from the left
ventricle through an imperfect mitral valve. Pre-
systolic thrill indicates obstruction afforded by a
narrowed mitral orifice to the current of blood issuing
from the left auricle.

We will conclude the subject of palpation by a
brief retrospect of the evidence which we have ob-

* German observers call this presystolic thrill, diastolic.

PALPATION.

tamed. Excluding negative and doubtful evidence,
you will observe that the sense of touch has given us
signs of great and positive value in the following
morbid conditions— atheromatous changes in the
arterial vessels— hypertrophy of the left or the right
ventricle ; dilatation of either of the ventricles ; peri-
carditis, in which it may have afforded evidence
as to the stage of the disease, whether there is
liquid effusion, whether the pericardium is rough-
ened, or whether old disease has resulted in ad-
hesions. Concerning valvular diseases of the heart
and their effects, we may have received evidence of
aortic obstruction from thrill ; of aortic regurgitation
from the locomotive pulsation of arteries, and, per-
haps, from diastolic thrill ; of mitral obstruction from
presystolic thrill, as well as from pulsation of the
left auricle; possibly of mitral regurgitation from
systolic thrill ; of tricuspid regurgitation from hepatic
pulsation.

We shall next consider the evidence to be derived
from percussion.

LECTURE IV.

PERCUSSION.

Increased resonance over heart — Increased dulness — Relations
of areas of partial and complete dulness — Pericardial effu-
sion— Cardiac hypertrophy and dilatation — Differential
diagnosis of the two conditions.

The object of percussion is to determine the size and
shape of the heart and its relation to the neighbour-
ing' structures. In my own opinion the best plan of
percussing- the heart region is to use the fingers only.
Place the fore and middle fmg'ers of the left hand
closely upon the surface of the chest, and tap with a
short, decided, but not violent stroke, and in no
hurried manner, with the ends of the fore and middle
fingers of the right hand. I consider that the fingers
of the left hand constitute the best pleximeter, and
the fingers of the right the best plessor. Thus we
obtain at the same time information by two distinct
routes : the ear obtains evidence of sound at the
moment that the tactile apparatus receives impressions
of vibration.

Proceeding by the method of exclusion we will
suppose that :

(«.) The precordial area is resonant — that is to say,
the percussion sound is clear and the vibration unim-
paired— there is no dulness. The most common cause
of this condition is emphysema of the lung. The
morbidly dilated pulmonary air-cells encroach over

PERCUSSION.

the area which, under ordinary circumstances, is
occupied by the walls of the heart. Moreover, the
heart may be pushed downwards by the too bulky lung-.
You may have been able, as I have indicated under
" Palpation," to feel the beating- of therig-ht ventricle
at the epigastrium.

A far less common cause of resonance over the
heart-region is the presence of air in the cavity of
the left pleura (pneumo-thorax). The tympanitic re-
sonance in this condition exists, of course, over the
whole of the affected side of the thorax.

In extremely rare cases, tympanitic resonance has
been found only over the situation of the heart and
pericardium ; it indicates the presence of air or g-as
in the pericardium (pneumo-pericardium), a condition
which may be induced by fistulous communication with
the lung-, the cesophag-us, or the stomach, or by the
decomposition of effused products of inflammation
within the pericardial sac.

We will now suppose that :

(b.) The precordial area is dull.— We shall have to
exclude, first, cases wherein the dulness is not to be
distinguished from that existing over the contiguous
thorax. Pleuritic effusion in, or empyema of, the left
side causes such dulness that the area of the heart
cannot be mapped out by percussion. If such liquid
effusion be in considerable amount, the heart may be
pushed completely to the right side, so that its apex
may be felt to beat under the right instead of under
the left nipple. Condensations of the left lung,
cancer, and abnormal growths in the thoracic cavity
also may make it impossible for us to determine by
percussion the outline of the heart. Assuming that
these interfering circumstances have been eliminated,

PERCUSSION.

we have now to consider the modifications of the
percussion-note induced by the heart itself.

We have already considered the normal topography
of the heart. We have now to remember that only a
certain portion of the heart, covered by its pericar-
dium, approaches close to the thoracic wall — a con-
siderable part being' overlapped by the borders of the
lung-. The portion of the heart which is uncovered
by lung- in conditions of health may be demonstrated
with sufficient precision in the following- manner : —
Draw a vertical line through the centre of the ster-
num. Mark a point A, on this midsternal line at the
level of the fourth left costal articulation. Note the
point B, where the apex of the heart is felt to beat.
Join A and B by an oblique line. Complete the right-
angled triangle by drawing a line from the heart-
apex, B, to the midsternal line at a point, C, just
above the ensiform cartilage, at the lower part of the
sixth costal articulation. The area enclosed by this
triangle will be the portion of heart which, in con-
ditions of health, is uncovered by lung. You should
compare it with the area on the thoracic wall occupied
by the whole heart as we have before described.

Now to percuss the heart-region. Begin by adapt-
ing the two fingers of your left hand held vertically,
nails upwards (we are, of course, still supposing our
patient to be in the vertical position, sitting or stand-
ing), to the thoracic surface, a little to the right of
the right border of the sternum. Aiter percussing
in this situation, advance the fingers nearer to the
midsternal line until the elicited sound is dull. Mark
the vertical line where dulness commences by a soft
pencil or by ink. In the next place commence to deter-
mine the left border of the dull area by percussing out-

PERCUSSION.

side the point of the apex-beat. It is more convenient
now to incline the fingers which are adapted to the
chest-wall obliquely, pointing- towards the sternum,
as the left line of dulness will be oblique. Mark the
line as previously. The upper limit of the dull area
is determined by percussing- from above downwards,
the fingers adapted to the chest-wall being held hori-
zontally. You have now obtained the upper and the
two lateral limits. The lower limit is not so easily
determined, because the cardiac merges into the
bepatic dulness. The heart and pericardium are close
to the left lobe of the liver, separated only by the
diaphragm, and I hold that the dulness over these
two organs cannot be discriminated. A line of dul-
ness, however, can be determined between the apex
on the left, and the commencement of liver-dulness
on the right, and you should join these points by a
line. For all practical purposes this procedure will
indicate to you the area of complete dulness over the
heart-region, the superficial cardiac region as it has
been called, and it demonstrates the portion of the
heart which is uncovered by lung.

But this is not all that is necessary. You should
now reverse the order of your procedure, and starting
from the line of dulness, make percussion farther and
farther outwards until the sound has the perfectly
clear character which it possesses over healthy lung.
I do not think it necessary to overburden you with
acoustic terms. To understand all that has been
written about percussion — sonoriety, pitch, clang,
timbre, intensity, tones, overtones, fundamentals, har-
monics, &c— one ought to be able at any moment to
conduct an orchestra, tune a harp, read music at
sight, and be equally versed in acoustics and prac-

PERCUSSION.

tical medicine. Some observers have made assertions
as regards the diagnostic power of percussion, that
others cannot help thinking extravagant; thus, it
has been said that it is possible to ascertain from the
percussion-note alone whether a heart has under-^
gone any fatty degeneration. It used to be told of
Piorry, when I attended his class, that he was able,
by knocking at the front door, to find out who was in
the drawing-room, but such a critical ear is not given
to everybody. Suflice it that the sound elicited by
percussion over the heart in the situations where the
lung overlaps it is modified by two causes — first, by
the nearness of a dense body (the heart) to the point
percussed, and secondly, by the existence between
the point percussed and this dense body of an air-
containing structure, the lung — i.e., an arrangement
capable of transmitting sonorous vibrations. As one
proceeds outwards the sound becomes less muflied,
and the vibration more manifest; but there is no
abrupt line of demarcation to indicate the outline of
the heart. Nevertheless, you should learn carefully
to note where the sound and vibration are uncom-
plicated (that is, where there is lung vibration only),
and where they commence to be modified. In esti-
mating the curves of this area, I think it is best to
employ as your pleximeter the little finger of the left
hand, placed laterally against the thorax, instead of
the fore and middle fingers. You should outline the
area with ink or pencil ; you will now have two con-
centric figures, the internal being the superficial
cardiac area which we have before noted, the external
the so-called " deep cardiac area " corresponding, if
it be carefully, and, I think I may add, fortunately,
ascertained, to the actual outline of the heart. For

PERCUSSION.

practical purposes I would advise you to realize these
two areas as, (1) the area of dulness, (2) the area of defi-
cient resonance, and it is the mutual relations of these
that you will find of diagnostic importance. The
breadth of (1) the area of dulness in health and in
adult life scarcely exceeds three inches transversely.
As regards (2), the sound in percussing- from above
downwards begins to be impaired about the third rib ;
a curved outline can be mapped out at this level to-
wards the right of the sternum, which indicates the
aorta, but you cannot separate the aorta from the
heart by percussion.

We will now assume that :

(c) TJie precordial dulness is extended upwards, and its
outline is of pyramidal or pyriform shape. Whenever
you find that dulness extends upwards above the third
rib, you have strong presumptive evidence of effusion
into the pericardial sac. If the sac is distended with
fluid you will find that the area of dulness extends
from the articulation of the first or second costal
cartilage, above to the sixth rib, or sixth intercostal
space below.

Here let me insist on the great value of charts or
diagrams as records of the physical signs of heart
diseases. These may be roughly drawn in a few
minutes, for sternum, clavicle, and ribs constitute
almost all the outlines that it is necessary to depict.
Be careful always to number the ribs as you outline
them. Blank chest-charts have been prepared by
many observers, and are extremely useful. You may
procure one in a few seconds by a rubbing from the
cover of this book.

Inspection and palpation have already indicated
points which should be recorded on the chart. The

PERCUSSION.

area of visible impulse should be outlined, the position
of the apex-beat and the locality of thrill or tactile
friction, if these exist, should be marked. Chalks,
or pencils of different colours, may be used with
advantage.

I have often found it of the greatest value to obtain graphic
records from the chest- wall itself ; for this purpose I use one
of Perry's copying-ink pencils, which I have found most con-
venient. The plan is valuable as an aide-memoire in all cases m
which a physical examination of the heart is made. You first
mark with the point of the pencil the spot of visible apex-beat ;
if this be extended, you denote the area of impulse by a dotted
outline. Then you mark, in like manner, any other points of
pulsation over the cardiac area, and proceed to further define
the outline by palpation ; afterwards the limits of precordial
dulness are traced out, and the positions and lines of con-
duction of murmurs, &c. The picture thus formed on the
chest-wall itself gives you a vivid summary of the evidence
which your physical examination has elicited. If you desire
to preserve a tracing, you should also make a dotted
outline of the position of certain of the costal cartilages, the
ensiform cartilage, and any other fixed points that you
may think necessary ; you then apply over the portion of the
chest thus marked, a piece of moistened tissue-paper. The
paper, of course, takes the markings made by the copying-
pencil, and you can thus preserve a permanent and exact record
of the physical signs in the case, and can compare it at
future times with tracings taken in like manner.

Now you will proceed to record the area of precor-
dial dulness. If this area be pyriform or pyramidal in
shape, with apex upwards, the probability is strong
that the case is one of pericarditis with effusion. We
will consider the signs that are confirmatory of this
view.

In the first place, the transition from dulness to
lung resonance is abrupt. As I have said, the normal
area of cardiac dulness widens gradually into pul-

PERCUSSION.

■monary resonance. The same occurs in many con-
ditions of disease, but where you have the pericardial
sac filled with fluid, the edge of lung', which normally
overlaps the cardiac area, is pushed aside, and the
area of deficient resonance (as opposed to dulness) is
done away with. The line between pulmonary reso-
nance and precordial dulness is well defined, more-
over the sense of resistance to the fingers on percus-
sion is increased ; vibrations are lessened.

In the second place, there may be noted a peculiar
relation between the area of dulness and the position
of the apex-beat. You may readily understand that
if the area of dulness which you have mapped out be
due not to liquid effusion but to enlargement of the
heart, you will feel the apex-beat at the lowest limit
of the dull area. Not so, however, when there is
effusion into the sac of the pericardium. Then the
apex-beat is tilted or floated upwards, and you get a
certain breadth of dulness between the apex above
and the stomach resonance below.

In the third place, you may observe that the extent
of dulness varies within comparatively short periods of
time. Effusion into the pericardium often takes place
rapidly, and you may find that the dull area which you
have mapped out previously, has, in a few hours, very
considerably increased. From day to day there may
be advances or recessions of dulness.

Again, in effusion into the pericardial sac the
dulness varies with the position of the patient. On
his lying down flat, the fluid subsides, then the apex-
beat again becomes evident, and the percussion note
becomes clearer, the lungs now returning to the
position whence they were displaced by the fluid.

These signs, then, assure us that there is fluid in

PERCUSSION.

the pericardium, whether due to pericarditis (the
other signs of which you will search for) or to passive
dropsy of the pericardium, which occurs, as I have

Fig. 1.

Showing the triangular area of normal cardiac dulness
and its relation to the hepatic dulness. The shading
indicates the area of deficient resonance— i.e., the deep
cardiac region.

said, with the manifestations of dropsy in other
situations.

The foregoing points may, perhaps, be better under-
stood by reference to the accompanying diagrams,
for drawing which I have to thank Dr. Stephen
Mackenzie.

Suppose now that :

(d.) The precordial areas of dulness a?id deficient rc-
smiance are extended laterally. The impairment of
resonance may be extended in either lateral direction.

PERCUSSION.

Assume (1) that it continues to the left of the border
of the normal triangle of cardiac dulness depicted in

Fig. 2.

Showing the pyramidal outline of dulness due to the
effusion into the pericardium, and the relation of the
heart to the distended sac.

Fig-. 1. This extension of dulness must be due either
to hypertrophy or to dilatation, or to both combined,
of the left ventricle. In hypertrophy you will have
already found that the apex beats below and perhaps
outside its normal position. The area of dulness will
be sharply defined, but it is only the extreme left of it
which will be much changed in outline. The base
line will be prolonged to the left of a line vertically
drawn from the nipple, and it will incline downwards
and towards the left instead of preserving its horizontal
position.

PERCUSSION.

In hypertrophy of the left ventricle, you will note
that the precordial dulness preserves its triangular
form, hut is prolonged towards the left side. You
will of course notice the expression of power m the
ventricular contraction, as evidenced to the eye, the

band, and the ear.

When the extension of dulness left of the normal
area is due to dilatation of the left ventricle, the out-
line is less angular and more rounded than It is in the
case of hypertrophy. The apex is less pointed and
more globular. The left border of the region also is
less defined; the area of deficient resonance is ex-
tended towards the left, and you will find the apex-
beat less powerful and less sustained, with the cha-
racter rather of a short and feeble slap.

As I have said before, hypertrophy and dilatation
often co-exist. As a rule, the more obtuse the outline
of the apex as obtained by percussion, the greater
the probability of dilatation, but the further discrimi-
nation between these conditions we shall consider
under " Auscultation."

We will suppose now the case that (2) the prtecor-
dial deficiency of resonance extends to the right of
the normal area. We have not, in this case, to de-
termine between hypertrophy and dilatation of the
right chambers of the heart, because practically the
two conditions always occur together.

You may (a) have no difficulty in discovering such
right side hypertrophy. You may find that the area
of absolute dulness extends beyond the right border
of the sternum over the cartilages of the third, fourth,
and fifth ribs, and when the right auricle is consider-
ably dilated, you may find dulness extend from the
second rib to the third intercostal space. In this case

PERCUSSION.

the enlarged heart has displaced the lung- which under
other conditions overlaps it.

Often, however, (Z>) the determination by percussion
of the outline of the right chambers is not easy.
Sometimes percussion over the precordial area elicits
no dulness at all. In such case the heart is over-
lapped by emphysematous lung, and it is precisely in
emphysema that dilatation of the right chambers is
apt to occur. Disorders of the pulmonary circulation,
involving as they do turgescence of the general venous
system, lead up to dilatation of the right (the venous)
chambers of the heart. Out of forty-five such cases
of secondary dilatation of the right heart, Lancereaux
observed twenty-four due to emphysema and chronic
bronchitis, and six due to respiratory trouble induced
by a malformation of the chest through rickets.
Though the area of absolute dulness may be abolished
in such cases, percussion, nevertheless, affords valu-
able data. You will be able to map out an area of
deficient resonance. Commencing well to the right of
the sternum, where the sound over the emphysema-
tous lung is imcomplicated, you will advance nearer
to the middle line of the sternum until you find that
the sound, though not dull, is impaired. Thus you
may obtain the outline of the deep cardiac area, and
closely approximate to that of the heart, covered as it
is by lung-. You will, of course, observe the con-
current signs — pulsation of the right ventricle at the
epigastrium, venous turgescence, perhaps venous
pulse, and, if the symptoms are advanced, oedema
spreading from the feet upwards.

We have now considered the evidence afforded by
percussion of dilatation and hypertrophy of the left
and right chambers respectively. You must, of course,

PERCUSSION.

be aware that the condition of enlargement may affect
both sides. In fact, dilatation of the right chambers
may follow from impairment of the propulsive force
of the left ventricle as consequence from cause. We
shall see this especially when we come to consider
valvular incompetence of the left heart. Suppose the
left ventricle to be dilated and enfeebled, it is obvious
that the first effect is a deficient propulsion of blood
through the aorta— the general circulation is impaired
owing to the reduced vis a tergo— the next result is
engorgement of the venous channels ; the right
chambers of the heart may be considered as part and
parcel of these venous channels — like the rest of the
venous system, they are in a state of habitual plethora,
so they become distended and enlarged, and their
muscle becomes hypertrophied.

Having learnt the chief lessons to be derived from
percussion of the precordial area, we shall in the next
lecture proceed to "Auscultation."

LECTURE V.
AUSCULTATION.

PART I.

Immediate and intermediate auscultation — Stethoscopes —
Normal heart sounds — Auscultation of voice to determine
area occupied by heart — Topography of the valves — Modi-
fication of normal heart sounds — Accent — Exalted second
sound, aortic and pulmonary — Strong pulmonary with weak
aortic second sound — Skoda's sign of mitral lesion — Strong
aortic second sound in renal disease — Prolonged first sound
— Short loud first sound — Reduplication of sounds — Ineffec-
tual systole.

I do not think it necessary to call your attention to
the importance of Auscultation. In the present day
this is fully recognized. I am not sure that there is
not a slight tendency towards an opposite danger — I
mean a too exclusive reliance upon the signs offered
to the sense of hearing. When the suggestion has
come that the heart-region shall be examined, I have
often observed that the stethoscope has been at once
flourished, and the listening over the prsecordium
finished, the diagnosis has been supposed to be mature.
I hope to have convinced you by the preceding lectures
that precious aids to diagnosis are neglected if auscul-
tation is alone relied upon.

On the other hand, the method of diagnosis cannot
be complete without auscultation.

Auscultation may be direct and immediate, or in-
direct and mediate.

AUSCULTATION.

(A.) Immediate Auscultation.— You may obtain some
general lessons by applying- the ear directly to the
heart-region, the chest being covered only by a fold of
linen. By this you will learn whether the heart is dis-
placed from its normal situation, and whether the sound
of its contraction is strong or feeble. If prolonged
and heaving you have corroborative evidence to add
to the signs of hypertrophy, which have been deduced
from previous examination. If feeble, you must hesi-
tate before concluding that the heart-muscle is weak,
for it is very probable that fatty tissue or emphyse-
matous lung may intervene between the heart and
your ear, and so occasion the feebleness of sound. If
loud and heard over a wide area — a wider area than
your examination by percussion of the space occupied
Dy the heart would lead you to suppose — it is very
probable that you have to deal only with functional
palpitation.

(B.) Intermediate Auscultation. — Immediate auscul-
tation is a useful preliminary ; it gives you certain
broad general impressions — but intermediate ausculta-
tion is absolutely indispensable. You have to dif-
ferentiate sounds coming from situations very close
one to the other. The valves of the heart all lie
within a square half-inch of surface ; if the tricuspid
be excluded, portions of all may be covered by a
superficial quarter of an inch. Practically, a sound
obvious enough at a given point, may cease to be
perceptible one-third of an inch therefrom. It is
obvious, therefore, that the unaided ear cannot be
relied upon, but that some means must be adopted
for collecting and localizing sounds. The stethoscope
must be used.

A few words as to the form of stethoscope most

AUSCULTATION.

suitable. The ordinary wooden stethoscope is the
most generally useful; the thoracic end should be
small enough to be adaptable to the intercostal spaces
in thin subjects. As a rule, I think the metallic stetho-
scopes are inferior.

The binaural stethoscope is extremely valuable.
For the cardiac auscultation of infants and children,
it is indispensable. Not only does it shut off from the
ears external sounds and allow the impressions to
come only from the part at which its cup is applied,
but its flexible collecting tubes allow each movement
of the patient to be followed. Otherwise, children
and infants may elude all your attempts at ausculta-
tion. Moreover, the sounds obtained through the
double tube of this stethoscope, transmitted as they
are to both ears, are perceived very intensely : sounds
may be heard which otherwise would be inaudible.
Still, I fully recognize that there is a danger — the
sound may be too intense, so that if two occur near
together, one may be drowned. The practical con-
clusion is, use ootli forms of stethoscope, the ordinary
and the binaural. I have my own stethoscope so con-
structed that the same cup and stalk can be screwed
into the ordinary wooden ear -piece, or into the
junction of the tubes of the binaural arrangement.*
" So I examine successively with each form of instru-
ment.

I have now for some time been accustomed to use
a form of binaural stethoscope, introduced, I believe,
by Professor Stern of Vienna. In this instrument
the spring which keeps the terminal cups applied to

* This has been made for me by Messrs. Maw, Son, and
Thompson.

AUSCULTATION.

93 •

the ears (and often when auscultation is long-continued,
causes inconvenient or even painful pressure) is dis-
pensed with. Each of the two india-rubher conducting
tubes has a vulcanite extremity, which " plugs " into
the auditory meatus, and with a little practice is easily
retained. The distal extremity of each india-rubber
tube plugs into a vulcanite cup, which is applied to
the chest. Messrs. Maw and Son have made for me
a modification of this instrument, with these advan-
tages :_(l) the distal extremities fit into a short
stethoscope made of vulcanite or wood, which, by
adapting an ear-piece can be used as an ordinary
stethoscope ; (2) the india-rubber tubing is graduated
in inches, so that the stethoscope serves also as a
cyrtometer, or chest measure.

' Now it is necessary briefly to consider the Normal
Sounds of the Heart. The mere application of
the ear to the prsecordium will convince you that the
noise of the heart in action can be resolved into two
sounds, which can be imitated by the syllables, hiVb-
dup. A little consideration will show you that the
first, the longer sound of lower pitch, is separated
from the shorter, sharper sound, by a short but dis-
tinctly appreciable interval of silence, and that, again,
a longer pause or silence intervenes between the
second sound and the recurrence of the first. Listen-
ing near the situation of the apex, you will find that
the first sound co-exists with the impulse of the heart
against the walls of the chest — that is to say, the
contraction of the ventricles, the systole.

Without entering in the spirit of criticism upon the
much-debated question of the exact mode of causation
of these sounds of the heart, we shall find it sufficient

for our present purpose to consider what is taking

AUSCULTATION.

place at the exact time at which these sounds respec-
tively are occurring-.

At the time of the production of the Jirst sound, the
following- are the conditions. The ventricles are full
of hlood. The auricles have just contracted, impel-
ling their contents through the auriculo-ventricular
openings, and completing- the replenishment of the
ventricles. Then the muscle of the ventricular walls
contracts — the tension of the enclosed blood forcing-
upwards the curtains of the auriculo-ventricular valves,
putting- them suddenly upon the stretch, and thus
closing- the orifices which they guard — driving the
blood contained in the ventricles through the only now
pervious openings — viz., the aorta on the left side, and
pulmonary artery on the right.

At the time of the production of the second sound
the conditions are these. The aorta, and through it
the arterial channels of the whole body, as well as the
pulmonary artery and its branches which carry venous
blood to the lungs, have just been filled with a gush
of blood. A momentary interval has occurred whilst
these onward currents have passed, and during which
the ventricles have commenced to become relaxed.
The blood has been forced by the systole not into
rigid tubes or into inert canals, but into the elastic
arteries. When, therefore, the ventricles have ceased
their contraction, and an appreciable pause has oc-
curred during which the impetus of the blood-current
has been unresisted, the semilunar valves of the aorta
and pulmonary artery respectively are suddenly closed.
The cause of such closure is twofold. First — the
mere weight of the superincumbent column of blood in
these great vessels ; secondly — the elastic recoil of
the previously stretched coats of the vessels of distri-

AUSCULTATION.

bution. In the case of the aorta, the elastic recoil
comes not only from itself, hut from every artery and
arteriole in the whole system — in the case of the
pulmonary artery, from the narrower limits of the
distributing- channels within the lungs. The second
sound, then, is short, sharp, and sudden, and there is
no doubt that it is due to the sudden closure of the
semilunar valves of the pulmonary artery and the
aorta.

During the pause following the second sound, the
heart muscle is flaccid, and the cavities are becoming-
refilled.

The first sound, then, is coincident with the con-
traction of the ventricles ; it is systolic. The second
occurs at the moment of closure of the semilunar
valves ; it is called diastolic, but it is obvious that it
occupies only a portion of the diastole. The diastole
of the heart embraces all that period which is not
occupied by systole.

Supposing the period of rhythm to be divided into
ten equal parts, the following expresses, according to
Dr. Walshe, the relative duration of sounds and
silences:

First sound = -4
First silence = "1
Second sound = *2
Second silence = "3

In commencing the auscultation of the heart's area,
you may have a duty as yet unfulfilled. Your former
investigation may have failed to have indicated the
situation of the heart's apex. This you must now de-
termine by means of the stethoscope ; observe and
mark the extreme left of the situation at which the

AUSCULTATION.

impulse is heard at its maximum ; that will corre-
spond to the apex.

It may be necessary also to employ auscultation as
a corroborative means of determining1 the area occu-
pied by (he heart, or by distended pericardium. You
do this by auscultating the voice. The lines where
vocal resonance terminates or becomes greatly dimi-
nished, indicate the border of the area.

We have now considered the necessary prelimi-
naries for Auscultation of the Heart. The apex has
been indicated, and the area occupied by the various
chambers has been mapped out. We have already
described the topography of the heart ; we have now
to consider the Topography of the Valves. The
aortic, pulmonary, and tricuspid valves all are situated
near the surface of thoracic wall- — not so the mitral —
this only approaches the surface at the point of the
apex-beat, where the left ventricle comes towards
the thoracic surface.

For the purposes of clinical investigation, the exact
anatomical delimitation of the valves is of less impor-
tance than the determination of the areas on the
thoracic surface to which the sounds proceeding from
them are conducted. There are four centres where
the sounds proceeding from the heart are determined
to the thoracic surface : —

At the heart's apex are heard the sounds produced
at the mitral valve.

At the lower end of the sternum, the base of the ensi-
form cartilage, the sound emanating from the tricuspid
valve.

At the second left intercostal space close to the sternum
the sound proceeding from the pulmonary artery.
At, the junction of the second right costal cartilage

AUSCULTATION.

with the sternum and the contiguous second right
intercostal space, the sound generated in the aorta.

As I have said, the area, as indicated hy the sound,
is not the absolute anatomical area.

1. " Sounds emanating from the mitral valve are not
looked for directly over the valve (in the second left
intercostal space, close to the sternal insertion of the
third left costal cartilage), as here the latter lies be-
hind air-containing lung tissue, a bad conductor of
sound ; they are auscultated rather at the apex of the
heart, which is free of lung, and in immediate contact
with the chest-wall, and towards which experience
shows that sonorous vibrations coming from the mitral
valve are transmitted with greatest intensity.

2. " In the same way the sounds of the tricuspid
valve are not to be sought for exactly over their point
of origin (behind the sternum at the level of a line
drawn obliquely from the sternal insertion of the third
left rib to the fifth right costo-sternal articulation),
but somewhat lower down on the lower portion of the
sternum."*

3. The sounds from the pulmonary artery are heard
best over its exact anatomical position : from its origin
in the right ventricle it rises to the lower border of
the second left cartilage, where it divides into its
right and left branches. The sounds from the vessel
are, therefore, best heard in the second left interspace,
where it is close to the thoracic wall.

4. " Sounds developed in the aorta are loudest, not
just over the orifice of the vessel (in the second left
intercostal space), but in the second right intercostal

* Guttmann, "Handbook of Physical Diagnosis :" New
Sydenham Society's Translation. London, 1879.

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space, in the direction of the ascending- aorta. As the
aprta at its origin completely covers the root of the
pulmonary artery, the sounds produced in these ves-
sels are necessarily intermingled, and would be indis-
tinguishable from each other, were it not for the fact
that those generated at the aortic valves are propa-
gated most energetically in the direction taken by the
current of blood in the ascending aorta, along the
course of the vessel towards the second right inter-
space ; at the latter point, therefore, aortic sounds
should be auscultated."*

Deferring for a time any consideration of abnormal
sounds heard over the heart's area, we will consider :

(a.) That the heart-sounds are modified
in degree.

A few words as regards accent. If you listen over
the apex of the heart, you will find that the more pro-
nounced of the two sounds is the first or systolic one.
The accent falls on the sound produced by the con-
traction of the ventricles, such sound more readily
reaching the ear. It would be expressed by the
syllables, liibb-dup. At the base, however, the accent
is reversed. The semilunar valves are nearer to the
ear, the accent falls on the shorter second sound and
the expression would be dup-lubl). This may give rise
in some cases to a little perplexity : you may take
the second sound for the first, and vice versa. The
difficulties may be obviated, however, by a very simple
rule. When you are auscultating the base of the
heart, place the finger over the spot of the apex-beat,
or, if this be too feeble to be distinguished, over the

* Guttmann, loc. cit. p. 262.

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situation of the great vessels at the root of the neck.
The impulse or the pulse will thus tell you which is
the first sound : of course if the sound you hear he
synchronous with the systole or pulse, it is the first
sound, if not it is the second. '•

It is well, in my opinion, to commence hy auscul-
tating- at the hase of the heart, because the situations
of the aorta and pulmonary valves are fixed points,
whilst the apex is variable.

Atthe base,in the absence of abnormal sounds,it is to
the second sound that you must pay attention. The qua-
lity of the first sound will be investigated at the apex.

You will place your stethoscope over the second
right costo-sternal articulation, then carry it across
the sternum to the second left interspace and the articu-
lation of the sternum with the third costal cartilage on
the left side. You will observe and compare the
qualities of the second sound in these right and left
situations respectively. The aortic second sound is
normally more pronounced than the pulmonary. It
is the closure of the aortic valves which gives, for the
most part, the character to the second sound which is
heard over the general area of the heart — that is to say,
the aortic overpowers the pulmonary second sound.
Suppose now that (a) the aortic second sound is intensified.
It is obvious that you must train your ear by observing
the second sound in cases of health. When you have
recognized its normal intensity only are you in a posi-
tion to judge of its exaggeration. If on placing your
stethoscope over the second right costo-sternal articu-
lation you hear a sharp and loud flap coming closely
to the ear, your inference must be that an abnormal
amount of blood, which has been forced into the aorta
by the contraction of the left ventricle, has, by the

h 2

100

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energy of its reflux, closed and put on the stretch the
semilunar valves. Carrying- your inference further,
you will find that you must have a strong, muscular,
in other words, hypertrophied left ventricle, and an aorta
capable of containing- an unusual amount of blood, in
other words, a dilated aorta. In conjunction, therefore,
with other signs, you will find persisted exaggeration
of tbe aortic second sound a valuable evidence of hyper-
trophy of the left ventricle. Conversely, if you find
that (b) the aortic second sound is feeble, you may infer
that there is a deficiency of arterial blood supplied to
the aorta by the ventricle. This observation is some-
times valuable as a means of prognosis when the blood
has been diminished in quantity by haemorrhage, or
when the tone of the heart has been enfeebled by disease.
In fevers a very weak second sound is a bad prognostic.
There are certain circumstances, however, which mar
or modify such absolute deductions from the observed
force or feebleness of the second sound. There may
be a sharp and loud second sound when the aortic
valves are unusually thin. Or it may have a dull or
leathery character when the valves are thickened. You
must, therefore, remember to record the observation,
but to make no absolute deduction without comparison
with other physical signs.

Suppose now that (c) the pulmonary second sound is
intensified. This is a sign of more absolute importance.
I have said that the great cause of intensification of
the aortic second sound is an increase above the
normal quantity of blood in the aorta. In case of the
pulmonary second sound another cause is present to
augment it. The pulmonary is a smaller circuit, and
the blood contained in it, like the water in a Bramah
press, exerts equal pressure in all directions. The

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101

blood-pressure in the general systemic circulation is
modified in various ways, by subsidiary circulations,
as the portal, and by many special conditions in the
various tissues. The pulmonary circulation may be
looked on as if conducted by a single flexible and con-
tractile tube from right ventricle to left auricle. If,
from any cause, therefore, there is any obstruction to
the flow of blood within the pulmonary circuit, the
result is not only congestion of the lungs, but also "a
uniform increase of the tension throughout the whole
of the pulmonary circulation, often accompanied, ii
long continued, by slight dilatation of the pulmonary
artery, and always by a closure of the semilunar valves
with an exaggerated force proportionate to the hin-
drance it has met with."*

Of still greater importance than the estimation of the
absolute strength or weakness of the aortic and pul-
monic second sound, is the observation of the relative
force of the sound in the two situations.

Suppose that you find that (d) the pulmonary second
sound is intensified whilst the aortic is enfeebled. Your
first inference will be, as I have just indicated, that
there is exaggerated tension in the pulmonic circula-
tion— that is the cause which must produce the exalted
second sound. This may occur, however, in any con-
dition of respiratory trouble when there is congestion
of the lungs, but then the second sound over the aortic
valves need not be perceptibly or persistently enfeebled.
The co-existence of a strong pulmonary with a weak
aortic second sound is a sign that whilst the pulmonary
artery receives too much blood, the aorta receives too
little. It is valuable evidence, as Skoda first pointed

* Balfour.

102

AUSCULTATION.

out, of a diseased condition of the mitral orifice either
permitting- regurgitation, or inducing obstruction of the
blood-stream. In the case of the former, the expla-
nation of the phenomenon is easy : the arterial current,
urged into the aorta by the contraction of the left ven-
tricle, is diminished by the amount which regurgitates
through the imperfectly-closed mitral orifice; the aorta,
thei'efore, is insufficiently supplied with blood, and the
sound caused by the reflux against its semilunar valves
is consequently weak. In the case of mitral obstruction
(stenosis) the effect is the same, though the cause is
different. Here the blood reaches the ventricle with
difficulty on account of the narrowing of the outlet from
the auricle, systole takes place upon an insufficient
amount, and the aorta is ill supplied. The case is just
otherwise with regard to the pulmonary artery ; as a
consequence of the deficient arterial supply, induced by
both the above conditions, there has been a reduction
of the rate of venous return, and engorgement of the
venous system, a secondary dilatation of the right side
of the heart. In regurgitation, a backward current is
created by the systole of the ventricle ; in obstruction,
the contraction of the auricle tends to cause reflux. All
these causes, therefore, produce high tension in the pul-
monary circuit. So, with the arterial antemia there is
venous and pulmonic hyperemia, and hence exaltation
of the shock of recoil of the semilunar valves pertaining
to the right heart. This observation of the comparative
intensification of the pulmonary second sound is valu-
able, not only as a sign of the existence of the conditions
I have just mentioned, but as an indication of their
degree— so it is of great importance in prognosis. In
proportion to the comparative feebleness of the aortic
second sound is the failure of the ventricle ; in propor-

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103

tion to its strength is the power of the ventricle, by its
compensatory hypertrophy, to overcome the obstacles
imposed.

If you find the opposite condition when (e) the aortic
second sound is relatively intensified, it is evidence, of
course, of hyperemia on the arterial side of the circu-
lation. I have already spoken of this as suggesting
hypertrophy of the left ventricle, but it is only to be
relied on in concurrence with other signs. There may
be much hypertrophy of left ventricle concurrent with
mitral regurgitation, when, as we have just seen, the
aortic second sound is enfeebled. In such case the
hypertrophy is insufficient to compensate for the loss
by regurgitation through the mitral orifice. Again,
though the left ventricle may be hypertrophied and
the aorta dilated, the coats of the latter (through
atheroma for instance) may be so inelastic that the
second sound may evidence no exaltation. There is one
condition of disease, however, in which accentuation
of the aortic second sound is a sign of considerable
importance — this is Chronic Bright's Disease. I have
called your attention already to the conditions which
exist in this disorder. There is a peripheral obstruc-
tion to the circulation of the blood through the ter-
minal arterioles, coincidently there is heightened
power of left ventricle ; the necessary consequence is
an abnormal excess of tension in the arterial system,
and this state of tension occasions the sharp and pro-
nounced aortic second sound.

It is important to note the relative predominance of the first
and second sounds at the base of the heart. You may find
that the first sound is nearly or quite inaudible, the only sound
is the diastolic. In such case there is strong presumptive
evidence of hypertrophy of the left ventricle.

We turn now from the base to the apex ; and our

104

AUSCULTATION.

consideration will be devoted to the first instead of
the second sound. Suppose we find that (J) the first
sound is abnormally prolonged. We have then evidence
of hypertrophy of the left ventricle. In auscultating
at the apex I advise you to keep distinct in your
minds the element of sound and the element of dura-
tion. You see that as evidence of hypertrophy I have
called especial attention to the latter. The first sound
is constituted by two factors, the contraction of the
ventricular walls, and the tension of the auriculo-
ventricular valves. The muscular sound of the con-
tracting ventricles is dull and prolonged, whilst the
sound of the stretching of the curtains of the valve
is (as you know it to be in the case of the semilunar
valves) sharp, short, and sudden. In proportion as
the muscular element of the first sound preponderates
over the valvular, so the first sound will be dull and
prolonged.

In hypertrophy the first sound is dull, partly because the
flap of the valve-curtains is less easily conducted lo the ear
through the thick muscle of the ventricular wall, partly
because the contraction of the ventricle itself produces a dull
(muscular) sound. It is prolonged, because the thicker the
muscle, the longer its period of contraction. (For a review of
the numerous theories as to the causation of the sounds of the
heart, see Hayden's "Diseases of Heart and Aorta," 1875,
pp. 93 et seq.) An able investigation on the question has been
made by Guttmann (see "Handbook of Physical Diseases,"
translated by Dr. Napier : New Sydenham Society, 1879,
p. 265, et seq.), who concludes thus : — "Although the whole
question in dispute cannot yet be said to be definitely settled,
the conclusion to which the present state of our knowledge
seems to point is, that the first sound is essentially of valvular
origin, and only to a slight extent muscular."

If on the other hand (g) the first sound is shortened,
it is evidence that the ventricle is weak. In this rela-

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105

tion we may have several conditions. The first sound,
though short, may be loud. It is rather a frequent
mistake to interpret loudness of the first sound as a
sign of increased power of the ventricle ; as a rule it
is the opposite. A loud, sharp, short, flapping- first
sound at the apex indicates dilatation, and consequent
feebleness of the ventricular walls* In such case
the muscular sound is reduced to a minimum, and the
ear appreciates in the greatest degree the valvular
element of the first sound. Then the first sound
approaches the second sound in character and dura-
tion. You may even be puzzled to discern the one
from the other. The following rule will easily guide
you : whilst you are listening by means of your
stethoscope, place your finger over the spot nearest
the heart apex, at which a decided pulsation is to be
felt. If the apex-beat is evident, place your finger
over its situation, if not, observe the carotid pulse
(not the radial, for that is fallacious, because it is not
always coincident with the cardiac systole). You
thus have a certain indication of the time of the systole,
and you will be able at once to know whether the
sound which you hear is synchronous with it — i.e.,
the first sound — or intermediate between pulse and
pulse, when it will, of course, be the second sound.
But the first sound may be short and yet feeble, and
this is evidence of a stdl graver condition of heart-
debility. You then have, not only an impaired mus-
cular sound, but a weak valve sound, for the enfeebled
muscle cannot create sufficient tension to produce the
pronounced flap of the valvular curtains. In such

* Such a first sound is met with in Graves' Disease. See
p. 30.

106

AUSCULTATION.

case you must look for the other signs and symptoms
of degeneration of the muscular walls of the heart.
In extreme cases of fatty degeneration, the first sound
may be lost altogether.

We will next consider briefly a condition which is
sometimes more interesting than important, but which
must always be noted and deciphered where it exists—
(/i) the sounds of the heart are reduplicate. Instead of the
single sound of the normal rhythm you hear two
sounds following as if the syllables tah-ta were uttered.
This may occur at the base or at the apex, or in both
situations. It may be heard as a permanent sign in
conditions of health, as a transient occurrence in such
conditions, as a permanent sign in disease, and lastly,
as a phenomenon, continuing definitely during a
morbid condition of the heart, and vanishing when
health becomes restored. On what does it depend ?
The inquiry is interesting, but the answer is not easy.
We will first take the case in which the phenomenon
is manifest at the apex and not at the base. Now I must
ask you carefully to discriminate between reduplica-
tion and ineffectual systole. I have already said that
in some cases contraction of the ventricles may be
repeated without producing a pulse to be felt at the
wrist ; so if you count the pulse at the wrist and
compare with the rate of pulsations as determined by
auscultating the apex, you find that the two records
do not exactly correspond.

Many cases and observations have been recorded
which illustrate this ineffectual working of the ven-
tricle, notably by Von Dusch, Potain, Hayem, and
Mint. This is not reduplication, however ; in re-
duplication there is a repetition only of a portion
(the systolic or diastolic sound as the case may be)

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107

of the cardiac revolution, whilst in ineffectual systole
the whole cardiac revolution is repeated once, twice,
thrice, or even four times, until sufficient arterial ten-
sion is attained to produce the pulse. In such case
the pulse may he sometimes felt in the larger vessels,
as the carotids, before it is manifest in the radials.
You may, perhaps, understand this better if I indicate
it graphically. Let the syllables tah-ta express the
cardiac sounds, tah being the first sound and ta the
second. Then Ineffectual Systole is thus re-
presented : —

tah ta tah-ta = Pulse : or
tah ta tah-ta : tah-ta = Pulse : or
tah ta tah-ta: tah-ta tah-TA = Pulse,
the latter indicating varying expressions of strength
of the sounds.

Reduplication of the First Sound is repre-
sented by

tah tah ta — Pulse : tah tah ta = Pulse, or
tah tah ta = Pulse : tah tah ta = Pulse.
A doubling of the first sound may be heard in health
at that period of the respiratory rhythm when expira-
tion has just been completed and inspiration is com-
mencing.

According to Dr. Hayden the phenomenon may
be associated (1) with simple functional derange-
ment of the heart, such as nervous palpitation and
fluttering, usually accompanied by ansemia ; (2) with
attenuation and weakness of the ventricles in persons
of middle age of nervous temperament ; (3) with a
weak degenerating heart, and dilated atheromatous
arteries ; (4) with simple hypertrophy of the ventricle.
According to Guttmann it may occur temporarily in
perfectly healthy persons; it may be noted at times

108

AUSCULTATION'.

m diseases of the heart— sometimes connected with
mitral, sometimes with tricuspid disorder — hut cannot
be said to be characteristic of any particular affection.

As far as regards clinical diagnosis, therefore, you
may conclude that the sign is of but little importance.
Of course you will in every case which comes before
you be careful to note it, because, as we shall see, its
investigation may have a strong bearing upon the
interpretation of some unsolved cardiac phenomena.

We will now consider reduplication of the second
sound, which is much more commonly observed. This
may be expressed by

tah ta ta = Pulse : tah ta ta = Pulse, &c.

Potain noted that reduplication of the second sound
occurred in health at the end of inspiration and begin-
ning of expiration.

It may take place in conditions of debility of the
muscular structure of the heart, and is often observed
in the course of typhoid fever, commencing usually in
the second week. In such cases M. Hayem has shown
that there is an inflammation of heart muscle. The
reduplication ceases as health is regained.

There is no doubt, however, that there is one con-
dition in which the phenomena occurs most frequently
and in its most pronounced degree — that is, in obstruc-
tion at the mitral orifice. Guttmann says it is heard in
almost a third of the cases of mitral stenosis, and Dr.
Hayden found it in thirty out of eighty-one. This
accords with my own experience. Of twenty-
seven instances of reduplicated second sound noted by
Dr. Haydeu, twenty-six were cases of mitral obstruc-
tion ; you will conclude, therefore, that doubling of
the second sound is a sign not only of physiological
but of clinical and diagnostic importance ; you will

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109

consider it as presumptive evidence of mitral stenosis.
Doubling of the second sound is also heard in cases of
adherent pericardium (Friedreich) occasionally, and
passim in engorgement of the right side of the heart,
in fatty degeneration, and in some cases of pulmonary
emphysema and of pulmonary tubercle ; and accom-
panied by murmur, occasionally in disease at the
aortic orifice. When you meet with it, note carefully
the area over which it is heard, and determine which
of its elements has the preponderance in given areas.
Dr. Hayden says : "In every example of this anomaly
which has come under my notice, the double character
of the sound was exhibited only in the area over which
the sounds of the aorta and the pulmonary artery were
both audible ; whereas when the stethoscope was shifted
a short distance to the right or left of this region, a
single second sound only was heard." * This does
not accord with Guttmann, who says : " The broken
diastolic sound is (so far as I have observed) certainly
not loudest over the large vessels, but at the lower
part, of the sternum and near the apex of the heart."f
My own observations accord with those of Guttmann.

There are few questions in cardiac pathology more difficult
than that of the mode of causation of reduplication of the
heart-sounds. This can scarcely be surprising when it is
considered that observers are by no means agreed as to the
causes of the normal, uncomplicated sounds of the heart. As
regards reduplication of the first sound, the theory of which long
seemed with greatest probability to be correct, ascribed it to
non-synchronous contraction of the two ventricles. Thus,
a right ventricular systole is followed by a left ventricular

* " Diseases of Heart and Aorta," p. 165.
T " Handbook of Physical Diagnosis :" Sydenham Society's
Translation, p. 27S.

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AUSCULTATION.

systole, or vice versd. Many observers have, however, found
it difficult to accept this theory on account of the structural
unity of the ventricles, and the observed consentaneousness
of their action. That such derangement of synchronism is pos-
sible is, however, some observers consider, well proved by
physiological research.

Dr. J. Barr, of Liverpool, considers that each side of
the heart has, to a certain extent, its own nerve-supply, and
can accomplish its own peristaltic action, and, though both
sides are set to the same time and have a complex interlace-
ment of fibres, "it is an experimental fact that one side can
begin or end contraction before the other.''* In some rare
cases, too, this want of synchronism on the part of the ven-
tricles can be clinically demonstrated. Dr. Barr has described
to me a case in which the impulse of the left ventricle could be
first felt, and then that of the right ventricle, and this suc-
ceeded by a weak impulse of the left. On auscultation there
were heard a loud systolic (mitral) murmur, then a sharp, clear
first sound, followed by a short murmur (mitral). The proxi-
mate cause of the reduplication then, as advanced by those
who first adopted the theory of asynchronous systole of the
ventricles was the retarded closure of the tricuspid valve,
owing to the excess of blood-pressure in the right cavities.
Dr. Barr, however, whose investigation of the subject is a very
careful one, whilst adopting the theory of asynchronism of the
ventricles, gives an opposite explanation of the proximate
cause. He considers that the excess of blood pressure in
the right heart (such as occurs in the normal heart during
deep expiration, when physiological reduplication of the first
sound is heard) stimulates the right ventricle to commence
contraction before the left, so the tense closure of the tricuspid
valves occurs before that of the mitral. One of the chief
objections urged against the theory of ventricular asyn-
chronism has been that the disturbance in systole ought in the
nature of things to be accompanied by disturbance in diastole,
that the non-simultaneous impletioh of the aorta and pul-
monary artery respectively should be followed by non-

* Vide a Paper on Reduplication of the Heart-Sounds,
Medical Times and Gazette, 1877.

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Ill

simultaneous closure, by reflux of the aortic and the pulmonary
semilunar valves ; that, therefore, doubling of the first sound
should invariably be accompanied by doubling of the second,
which is not the case. Dr. Barr meets this difficulty by ad-
vancing the view "that though the right ventricle commences
its systole before the left, it is longer in emptying itself,
owing to its overloading, and to the increased obstruction in
the pulmonary circuit, hence, although it had the start of
the left, it has not completed its contraction before it, so there
is no reduplication of the second sound under these circum-
stances." Of other theories which have been advanced to
explain reduplication of the first sound, may be mentioned
that of Guttmann, which ascribes it to non-synchronous
tension of the individual segments of the auriculo- ventricular
valves owing to absence of perfect uniformity in the con-
traction of the papillary muscles. This hypothesis appears to
me in the highest degree improbable; it would seem much more
likely that such irregularities on the part of the papillary
muscles could produce, not reduplications, but murmurs. Dr.
Hayden's view is, that the doubling is equivalent to the resolu-
tion of the first sound into its two constituent elements — viz.,
the ventricular impulse and the click of valvular tension.
According to this, the click of valve tension should occur at
the very latest period of systole, the "thud" of muscular
impulse always preceding it. This cannot, however, be sus-
tained, for cardiographic evidence abundantly shows that the
closure of the auriculo- ventricular valves occurs early in the
systole, and that the first sound is prolonged subsequently to
their closure. The ' ' click " therefore ought always to precede
the "thud," whereas Dr. Hayden says that, in his experience,
without exception, " the first element of the double sound has
been didl and muffled, and the second sharp and clear."*

Dr. George Johnson has advanced a theory totally distinct
from the others. He considers that the so-called reduplicated
first sound consists of really the rapidly following sounds of first
an auricular and then a ventricular, systole. The contraction of
a dilated, and especially of a hypertrophied auricle becomes
audible, and the first division of the double first sound is the result

* " Diseases of Heart and Aorta," p. 118.

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AUSCULTATION.

o f the auricular systole. That the sound can be the direct effect
of the systole of the auricle is very difficult to believe. As
well as other observers I have had opportunities of auscultating
the auricle in very many conditions of dilatation aDd hyper-
trophy, and when it has been through pulmonary disease
totally uncovered by lung, but in no case has there been a
particle of evidence that its muscular contraction is accom-
panied by sound. Nor does it seem probable, when we
consider how feeble is the muscular sound of the ventricle,
even in conditions of the greatest hypertrophy. Whilst
denying that the sound is the direct effect of the auricular
systole, I would by no means assert that it may not be the
indirect effect thereof. It is quite conceivable that in some
cases the energetic systole of the auricle suddenly floating up
the curtains of the mitral valve, may so put them on the stretch
as to cause a sound— the click of valve-tension. Potain noticed
a form of seeming reduplication of the first sound, which he
termed " bruit de galop " in cases of hypertrophy of the heart
associated with granular kidneys. He considered that the
first element of the apparent reduplication was presystolic.
Guttmann also has observed such presystolic sound in a
number of cases of cardiac hypertrophy ; he considers that the
auriculo-ventricular valves are to a certain extent rendered
tense at the end of diastole— that is in the presystole ; but this
tension is so feeble that no sound results ; when, however,
from hypertrophy of the auricle the tension is increased, it is
quite possible that sound may be occasioned.

As I have said, reduplication of the first sound is a pheno-
menon of comparative rarity. Many good observers have
never met with a case. Dr. Hayden has noted twelve
examples— eight in cases of females, four in males. Of
these, six were considered nervous ; three associated with
menstrual disturbance; one with gout; another with Graves'
disease. Hypertrophy of the left ventricle existed in three
cases ; dilatation (in connection with cirrhosis of the liver) in
one case ; and fatty degeneration in two cases. Mitral
stenosis existed in one case ; in this both sounds were
double.* Dr. Hayden says : " Reduplication of the first
sound is so intimately associated with simple or eccentric

* " Diseases of Heart and Aorta," p. 164.

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113

hypertrophy that, if carefully sought, it will be found iu every
such case anterior to consecutive degeneration of tissue." I
have already said that I can by no means accept Dr. Hayden's
theory of a splittin°-up of the normal first-sound into its two
component elements of muscular susurrus and valve tension
It appears to me that either («) the reduplication is real and
caused by non-synchronous tension of tlm aurieulo- ventricular
valves of the right and left sides, or (6) it is only apparent and
due to a presystolic being closely followed by a normal first
sound, the presystolic sound being produced by the sudden
floating upwards of the mitral curtains, occasioned by the
auricular systole. I have met with reduplication, or apparent
reduplication of the first sound in eleven cases. Of these the
conditions were various, but classification could, in my opinion,
be made as follows: — (a) cases (four) in which there was
evidence of prolonged ventricular systole, with rough first
sound or murmur (in one case double murmur) at the base of
the heart, aad a pulse of decidedly high tension ; (b) cases
(three) in which there was a disturbance of respiration and
evidence of, at least temporary, distension of the right chambers
of the heart ; (c) cases of mitral stenosis (three) ; (d) one case of
myocarditis in course of typhoid fever ; here both first and
second sounds were doubled. The positions of audibility of
the reduplication were over the apex, five cases ; over theba3e,
two cases ; generally over the praecordium, one case ; over the
right cavities, one case ; and in two cases its audibility varied
from apex to base. In a, b, and d, it would seem quite pro-
bable that the theory of asynchronism of the pulmonary and
aortic second sounds might be justified ; but in group c, it
appears to me that there are strong probabilities that the
apparent reduplication is really a presystolic succeeded by a
systolic sound. This view may be best illustrated by the
following brief abstract of a case: — Female, aged thirty,
admitted under my care at the London Hospital, for epilepsy.
Subacute rheumatism occasionally from age of six. Pregnant.
The physical signs as regards the heart showed briefly the
apex in normal position ; first sound subdued but accompanied
by murmur conveyed towards axilla. At base, second sound
pronounced, but no other abnormality. On the day follow-
ing admission, I found that the first sound was reduplicated,
the reduplication was heard in a line leading from the fourth

114

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interspace to the anterior border of the axilla. Two days
afterwards the patient aborted. The reduplication persisted
but changed in certain characters, at the end of a fortnight it
was heard from the third interspace to the apex ; a little
internal to the apex reduplication was distinct and sounds
uncomplicated. On nearing the apex a soft systolic murmur
tailed off from the second element of the reduplication, and at
the apex, reduplication was lost, a first-sound murmur only
being heard. Sphygmographic tracings gave evidence of hyper-
. trophy of the left ventricle ; there was an ample tidal wave
and the dicrotic was high in the tracing. The trace also
showed occasional disturbance of rhythm (double pulse), and
the diastolic periods were unequal in time. Cardiography
evidence confirmed this diagnosis of hypertrophy. In some
tracings there was evidence of the point of closure of the
auriculo-ventricular valves ; the summit of the systolic portion
was broad, and the terminal swelling marked. In the diastolic
portion, the auricular eminence was chiefly remarkable for the
breadth of its base. This case tells in favour of the view that
the second element of the reduplication was the voice of the left
ventricle. This is shown by the fact that the murmur which
started from it was mitral systolic. To what then was due the
first element ? It seems scarcely likely that it could be the voice
of the right ventricle— of the tricuspid valve— for reduplica-
tion was at first not even audible over the right ventricle. It
would seem to me more probable that it was due to the
presystolic flap of the mitral valve in the manner I have before
mentioned. This view was,' I think, confirmed by the progress
of the case ; for, after losing sight of the patient during the
interval, I had an opportunity of examining her again eight
months subsequently, then there was no reduplication of the
first sound but a presystolic murmur, typical and distinct. I
am convinced that in certain cases of mitral stenosis a phe-
nomenon closely or exactly simulating reduplication of the
first sound may be observed. (See Part II.) In one case
of mitral stenosis, in which I noted this close resemblance to
reduplication of the first sound, tbe cardiography tracing
showed a very broad, pronounced eminence, indicating the
auricular systole; the inference was plain that there was much
hypertrophy of the auricle and the degree of stenosis slight, so
that the auricular contraction gave a distinct impulse to the

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115

apex. The mechanism of production of such sound seems to
me by no means difficult to realize. During the interval imme-
diately succeeding the relaxation of the ventricle, the blood,
subject to the tension in the left auricle and pulmonary veins
has been pouring into the ventricular cavity; the fluid
naturally finds its way in the direction of least resistance, that
is, its course, when impelled towards tbe apex, is round the
walls of the ventricle, thus coming behind the curtains of the
mitral valve, and bellying them out (so to speak) as the sails of
a ship are bulged by the force of the wind. At the moment of
auricular systole, the ventricle, as yet only partially full, is
rapidly distended, the force of contraction of the auricle
giving an impulse to the apex of the ventricle, and, as may of
course be inferred, giving a contre-coup to the already
partially-strained mitral curtains. In normal conditions such
contre-coup is inaudible, but when the auricle is more thau
ordinarily powerful, or when the mitral valve is so changed as
to give rise to the sound of membranous tension, it becomes
perceptible closely preceding the soimd produced by the ven-
tricular systole— that is, the sound of complete closure of the
valves guarding both auriculo-ventricular orifices plus the
muscular sounds of the ventricles. The sharp, short, first
sound so common in mitral stenosis I believe to be chiefly due
to sudden tension of the tricuspid valve. In this I know other
observers, especially Dr. Barr, agree with me. I would by no
means urge, however, that such must be the universal inter-
pretation of cases of reduplication of the first sound. Infre-
quent as are the instances, their very incongruity teaches that
each case must be judged for itself. For cases of physiological
reduplication, Dr. Barr's theory offers, to my mind, a plausible
explanation. So also it may explain others connected with
neurotic disturbance. I find it difficult, however, to associate
reduplicate first sound in any causal way with differences
of intra- ventricular pressure, seeing that long-persisting varia-
tions in such pressure and disturbances of balance must be so
common, whilst the phenomenon itself is so rare. As regards
its probable auricular origin, in some cases we may get
more evidence in our consideration of reduplication of the
second sound. A reference to A. B. Pig. 3 will show the
mutual relations of these reduplications. Now supposing it
were granted that the sound-producing tension of the mitral

i 2

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curtains might be effected iu some cases early in diastole, and
not only always late iu diastole — tbat is, in presystole — we

Fig. 3.

Diagram showing positions in the cardiac rhythm oiapparent
reduplications of A the secoud, B the first sound.

might have in some instances a semblance of reduplication of
the first, in others of the second, sound. If the tension
happened to be effected late, or in presystole, it would be
represented by B. in the diagram —apparent reduplication of
the first sound ; if early, by A, apparent reduplication of the
second sound.

So-called reduplication of the secoud sound is a phenome-
non which observers agree to be much more frequent than that
we have just considered. It is undoubted that by far the most
common condition in which double-second sound is heard
is mitral stenosis. Next in point of frequency, according
to Dr. Hayden, is aortic insufficiency. With considerable
unanimity the phenomenon has been ascribed to a want of
synchronism in the closure of the valves of the aorta, and of the
pulmonary artery respectively. The sequence of closure may
vary. In cases of aortic insufficiency, Dr. Hayden is satisfied
that the second element is aortic, because the murmur of
aortic regurgitation accompanies it. He believes that in such
cases the left ventricle is dilated, and so is slower to become
emptied in systole ; consequently the aortic reflux is post-
poned. On the other hand, in mitral stenosis the derange-
ment is chiefly in the pulmonary artery, "the entire pul-
monary system and the right chambers being engorged by
obstruction at the mitral orifice. In the effort to overcome
this obstruction, the systole of the right ventricle is pro-
tracted, and the reaction of the pulmonary artery proportion!

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117

ately postponed. The reaction of the aorta is, on the other
band, in mitral stenosis most probably anticipated, where the
left ventricle is reduced in capacity, as always is the case
where mitral or aortic reflux does not co-exist. Hence it is
likely that in simple mitral stenosis two causes of doubling of
the- second sound are in operation— viz., diminished capacity
of the left, and dilatation of the right, ventricle " (" Diseases
of Heart and Aorta," p. 128). It seems a truism to assert
that conditions of blood-pressure in the two great vessels
respectively, cannot be the vera causa of such reduplication ;
for until tbe occurrence of diastole, there can be no reflux,
and consequently no second sound. The causation of redu-
plication, as of the first so of the second sound under the
theory we are now discussing, must revert to the ventricles.
When their systole is simultaneous, the second sound, pro-
duced by reflux against the semilunar valves of the two great
vessels, at the moment of their relaxation, must be simul-
taneous also. When their systole is not simultaneous, or does
not last through equal periods, the diastolic reflux cannot be
simultaneous ; if the discrepancy be such as can be appre-
ciated by the ear, the second sound is doubled. The following
is Dr. Barr's view: — "As I have ascribed reduplication of
the first sound to asynchronism in the initial stage of ventri-
cular contraction, so I believe reduplication of the second
sound to be due to asynchronism at the end of contraction,
and in the consecutive reaction of the aorta and pulmonary
artery, with the tension of their respective valves." The
comparative rarity of cases of reduplication of the first sound
is explained, by Dr. Barr, by the much greater length of time
occupied by the first than by the second sound, whence is
required a correspondingly greater want of synchronism
between the closure of the tricuspid and mitral valves than
between the pulmonic and aortic, to produce a reduplication.
Physiological reduplication at the end of inspiration is
accounted for by the fact that the capacity of the pulmonic
system being increased, the obstructive burden upon the right
ventricle is lessened, consequently the systole of the latter
is shortened. The lessening of the duration of the systole of
the right ventricle implies anticipation of the diastolic closure
of the pulmonary semilunar valves — so there is a reduplicate
second sound, the primary element being pulmonic. In

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AUSCULTATION.

pathological reduplication, the origin may be in either the
right or the left ventricle. If from any cause the systole of
one of the ventricles be protracted, the diastolic closure of
the valves of its great vessel of exit will be delayed also, and
so the second sound will be double. Guttmann supports the '
view of non-simultaneous closure of the aortic and pulmonary
valves, without giving reasons for the proximate cause. He
says, however, that it is not unreasonable to explain the phe-
nomenon by a change in a single set of the semilunar valves,
causing their tension to take place in two distinct moments.
This hypothesis appears to me impossible to accept; such
change would surely be likely to produce murmur rather than
reduplication. But Guttmann says that reduplication of the
second sound in mitral stenosis is difficult to account for satis-
factorily, and in this I quite agree with him. He adds :
' ' The broken diastolic sound is (so far as I have observed)
certainly not loudest over the large vessels, but at the
lower part of the sternum, and near the apex of the heart,
and is further absent in those more marked cases of mitral
contraction, precisely in the cases in which the conditions
most favourable to the postponement of the closure of the
pulmonary valve are present in their highest degree." Redu-
plication, moreover, does not occur in mitral regurgitation
where the conditions of relative blood-pressure are profoundly
altered. Guttmann considers it probable that the redupli-
cation may arise at the narrowed mitral orifice itself ; that it
may be a component part of a presystolic (or, as he terms it,
diastolic) murmur, and adds that it has been conjectured that
the first element of the reduplication is the diastolic pulmonary
sound, and the second is produced towards the end of diastole
by the contraction of the hypertrophied left auricle (" Physical
Diagnosis," p. 279). In fact, the hypothesis reverts to the
last I have mentioned as probably explaining some cases of
reduplication of the first sound. I consider then that there
is a theory of auricular causation of reduplication of the
second sound which is well worth considering aud that we
have before tis two plausible explanations of the pheno-
menon ; —

A. That it is due to non-simultaneous closure of the semi-
lunar valves in the aorta and the pulmonary artery respec-
tively.

AUSCULTATION.

B. That it is the effect of a sudden tension of the mitral
curtains after the normal second sound.

I now proceed to discuss the evidence on this question,
which my own cases have afforded me. As I have said I
have observed reduplication of the second to be far more fre-
quent than that of the first sound, and in a vastly prepon-
derating number of cases the phenomenon is associated with
mitral stenosis. It has occurred in about a third of the cases
of mitral stenosis which I have examined ;* it would therefore
appear d priori probable that in this form of valve-tension
there should be some special reason for its occurrence. I will
consider first the evidence of my cases of reduplication of
second sound in conjunction with mitral stenosis.

The following case is illustrative :— A lady of fifty was fre-
quently under my care for symptoms of dyspepsia ; there was
no history of rheumatism nor development at any time of
articular phenomena. I had frequent opportunities of ex-
amining the heart, but found no lesion. After a few months,
however, during which no special symptoms had manifested
themselves, the patient complained of fluttering of the heart,
and I then found a rough presystolic murmur just internal to
the apex, with a short systolic murmur heard at and outside
the apex. There was distinct reduplication of the second sound
heard at the aortic cartilage and down the left border of the
sternum, but ceasing at the point internal to the apex, where
the presystolic murmur became audible. At the next exami-
nation the reduplication was heard as far as the apex. A sub-
sequent note states, "reduplication very marked, but no
presystolic murmur heard." Afterwards, " no reduplication
heard at any part of base ; commences well below the region
of the pulmonary valves, and is certainly loudest at or eyen a
little outside the apex." A subsequent note : " Reduplication
still very pronounced ; not heard at left base nor anywhere
left of the sternum until the level of the fourth costal car-
tilage ; it is well heard at the apex, and marked in the axilla."
Afterwards it was audible at the left scapula.

We will ask now whether these phenomena can be explained
by the theory which postulates want of synchronism between
the aortic and the pulmonary second sounds. Supposing this

* Strictly speaking, eleven cases in 37.

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AUSCULTATION.

theory to be correct, it would be the aortic that would be the
first element of the reduplication ; because, as the aortic
region was receded from, the second element of the reduplica-
tion undoubtedly became more and more pronounced. But
to accept this theory even under the conditions first noted, we
must agree that the aortic second sound was very loud, not
only over its normal area, but as far as the apex. We had in
this case, however, abundant reason for knowing that the
aortic tension instead of being above was far below the
normal. A reference to the record of one of Dr. Hayden's
cases points to the same difficulty. Here "the second sound
was double, and heard all over the prascordium." Under the
accepted theory, therefore, the aortic second sound, its first
element, must of course have been audible all over the
prsecordium, that is, over a wider area than often the normal
aortic second sound is heard. But the case was well
observed and diagnosis confirmed by post-mortem exami-
nation, and Dr. Hayden adds : " The quantity of blood, which
in this case, passed into the aorta at each systole of the
left ventricle must have been very small, owing to the twofold
lesion of mitral obstruction and incompetency." Moreover,
the aortic orifice was reduced to the diameter of the point of
the little finger, and its valves thick, and therefore less dis-
posed to give the " click " of closure. The difficulty of accept-
ing the asynchronism theory is further greatly increased by
consideration of the subsequent areas of audibility, for
the reduplication was not even audible in the aortic area.
On the other hand its area of audibility became nearer to
the apex, and afterwards included, not only the apex, but
the region of the axilla external to it and even the back.
Seeing, therefore, that the reduplication was manifest in areas
in which even the normal aortic second sound is often
inaudible, I conclude that, in this case, the latter could have
had no share in producing the phenomenon of reduplication.
In not more than half the cases of reduplicated second sound
iu mitral stenosis which I have observed, has such reduplica-
tion been audible in the aortic regiou. It is almost invariably
heard best down the left border of the sternum up to the
point at which the presystolic murmur becomes manifest.

It seems to me, therefore, that reduplication of the second
sound in cases of mitral stenosis can be best explained thus :

101

AUSCULTATION. AwA

The first element of the reduplication is the normal second
sound ; the tension in the aorta being feeble, it is the puhnomc
element which has the chief share in the production of sucn
second sound. The second element of the reduplication is the
sudden tension of the abnormal mitral-curtains produced alter
the relaxation of the left ventricle. I am not prepared to say
that systole of the auricle is essentiai to produce this sudden
tension ; it may be quite possible that the reaction of the dis-
tended pulmonary veins and left auricle may be sufficient to
cause it. So it may occur previously to the auricular contrac-
tion, the latter occasioning or reinforcing the presystolic
murmur, separated by a slight interval from the second element
of the reduplication.

I will now consider the evidence in the cases of reduplica-
tion of the second sound, which I have met with not in asso-
ciation with mitral stenosis. Of such there were eleven
examples, which I consider could be ranged under two cate-
gories. L Cases in which there were troubles of respiration
(broncho-pneumonia, phthisis, dilatation and signs of failure
of the left ventricle, and especially dilatation of the right
chambers of the heart). In this class were eight cases. It
is noteworthy that in all in which the area of audibility of the
reduplication was noted, this was either that of the origin of
the pulmonary artery or else of the apex of the right ventricle.
In this respect, therefore, the cases were strikingly dissimilar
from those in which the reduplication was associated with
mitral stenosis. I am quite disposed to think that the theory
of asynchronism of the two second sounds would best explain
them, and that Dr. James Barr's view as applied to explain
the physiological doubling of the second sound— i.e., the
assumption that the systole of the right ventricle is shortened—
is in these particular pathological conditions probably correct.
The other class in which I have found doubling of the second
sound in the absence of mitral stenosis is: — II. Cases in which
there was hypertrophy of the left ventricle, with high tension
in the arteries. In these it is to be noted that the area of
audibility of the reduplication was more variable, more exten-
sive, and especially approached the apex more closely than in
those of the former group. In the case of a female, aged
fifty, with chronic renal disease and hypertrophy of the left
ventricle, the reduplication, as observed at different periods

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AUSCULTATION.

was, (1) the heart's apex ; (2) base as well as apex ; (3) base
only and maximum in aortic area. Post-mortem examination
showed great hypertrophy and dilatation of left and right
chambers. In the three cases in this category it would be
quite legitimate to infer that there was protracted systole of
the left ventricle, and that the right ventricle having more
quickly accomplished its contraction, reflux against the pul-
monary valves took place at an earlier period in diastole than
reflux against the aortic. Such would accord with Dr. Barr's
theory, and a case which I had an opportunity of closely
observing, convinced me that if there were such asynchronism,
the pulmonary second sound was the first element of the
double sound. Whilst the probabilities are here also in favour
of the theory of asynchronism, I think it not impossible that
the phenomena may be explained by my theory of diastolic
tension of the mitral curtains as in the cases of mitral
stenosis. On this point we require more evidence. As prac-
tical points I would urge that in any case which seems to
present reduplication of the sounds of the heart, you should
endeavour with care to establish whether such reduplication
is real or apparent. Remember that reduplication of the first
sound may be simulated by a presystolic sound occasioned
(as I have described) by the systole of the left auricle. In
apparent reduplication of the second sound, remem ber that
there is presumptive evidence of mitral obstruction ; in a
minority there is a disturbance of rhythm owing to comparative
feebleness of the right ventricle, or to hypertrophy with slow
contraction of the left.

You will meet with many instances of disturbed
rhythm of the heart which are exceedingly puzzling-,
but by attention and repeated examinations you will
be able to resolve them in most cases. A tumultuous
and irregular succession of sounds, which at first seem
chaotic, may frequently be analysed, and found due to
a definite association of morbid and normal heart-
sounds.

LECTURE VI.

AUSCULTATION.

PART II.

Abnormal sounds— Pericardial friction-sound— Relations be-
tween pericarditis, rheumatism and renal disease-
Influence of posture on friction-sound — Exocardial friction
— First sound murmur over aortic valves — Anaemic mur-
murs—Murmurs in chorea— Aortic stenosis— Ulceration of
aortic valve-segments— Aortic second sound murmur — Evi-
dence from ophthalmoscopic examination — Aortic insuffi-
ciency— Physical cause of murmurs — Conduction and con-
vection of murmurs — Double aortic murmur.

Having considered the modifications of the normal
sounds, we will now turn to our second subdivision
and assume : —

(b.) That abnormal sounds are heard over

THE HEART REGION.

Abnormal sounds, heard at, or close to, the situa-
tion of the heart, acompanying' the cardiac movements
and apparently mingling" with some of the normal
sounds, may have their origin (1) in the structures ex-
ternal to the heart and pericardium ; (2) in the peri-
cardial sac ; (3) in the muscular tissues of the heart ;

(4) in the endocardium and the valves of the heart ;

(5) in the blood transmitted by the heart.

As regards the first-mentioned cause of abnormal
sound, it is of course assumed that you have carefully
estimated the pulmonary conditions, especially of the

AUSCULTATION.

left cavity of the thorax and the lung- which borders
on the heart region. The diseases which you have
chiefly to consider as inducing sounds which resemble
those due to intrinsic diseases of the heart, or as modi-
fying and irregularly conducting the sounds due to
intrinsic diseases, are pleurisy with viscid effusion,
cavities in the pulmonary substance near the heart,
and condensation of the lung. The differential dia-
gnosis of these conditions we shall consider as occa-
sion arises.

We will assume that :

(1.) A rubbing or creaking sound, accompanying
both movements of the heart, is heard superficially
over the cardiac region, but is not intensified at apex
or base.

This indicates a diseased condition of the pericar-
dium in which the visceral and parietal layers are
separated by a viscid or fibrinous effusion, or in which
the pericardium itself has become thickened or rough-
ened. Your previous examination may have given
a clue to your diagnosis. You may have con-
cluded that the pericardial sac is more or less dis-
tended, and the symptoms may have assured you that
there is in existence a pyrexial disease accompanied by
cardiac, pulmonary, and, perhaps, cerebral phenomena.
You may even have had the more positive evidence of
pericardial friction fremitus. Moreover, you may have
heard the friction-sound by direct application of your
ear to the chest before commencing- to use your stetho-
scope. If you suspect pericarditis you should, in my
opinion, never omit the method of direct auscultation.

But you may have none of these signs to guide you,
and let me insist strongly on this. Your patient may
have pain referred to some of the joints ; these pains

AUSCULTATION.

125

may be very trivial in character, may, indeed, be
absent ; pyrexia may be very slight or inappreciable.
I mentioned in an early Lecture a case of pericarditis
in the most pronounced degree which went through
its course without a single symptom of distress. I
have lately had under my care, at the North-Eastern
Hospital for Children, a boy who manifested the
disease with its grave progressive course and compli-
cations, but with the occurrence of so few subjective
symptoms that it was impossible for me to persuade
the parents to leave the child as an in-patient, and he
was brought to me bi-weekly as an out-patient. In
this case there was loud pericardial friction, which, as
it faded away, gave place to the murmur of mitral
regurgitation, indicating that "endocarditis had at-
tacked and spoiled the mitral valve ; at the next con-
sultation it was evident that the disease had spread to
the aortic valves, for there was a murmur of aortic
obstruction, and at the following there was, in addi-
tion, a murmur of aortic regurgitation, showing that
the endocarditis had rapidly destroyed the integrity of
the aortic valves and induced their most dangerous
lesion. You will remember, then, that you are not
to look for pronounced symptoms to suggest to you
the occurrence of pericardial friction.

T have said that your patient may complain of pain
in one or more of the joints. This rule you are most
strongly to observe — carefully to examine the heart
and to suspect pericarditis in any case manifesting
acute or subacute rheumatism. By far the most com-
mon form of pericarditis is that which is associated
with rheumatism. Many circumstances govern the
frequency of the manifestation of pericarditis in rheu-
matic fever, and authors vary in their estimate of such

12G

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liability even from 16 to 37 per cent. I have com-
pared the figures recorded by Fuller, Von Bamberger,
Roth, Leudet, Duchek, and Chambers, and I find
that they give about 24 per cent, as the ratio of cases
of pericarditis occurring in acute rheumatism.* Of
50 cases of recent pericarditis, Flint observed that 19
were manifestly rheumatic. Even this high figure,
however, does not represent the prevalence of the
rheumatic form of pericarditis ; for I have already
drawn your attention to the fact that pericarditis
occurs in the subacute form of rheumatism, and in
cases where the articular phenomena are very slightly
developed. In some rare cases the process of rheu-
matic fever commences by pericarditis.

Another condition of disease in which you must
recollect that pericarditis is probable, is renal disease.
In all cases of pericarditis, but especially in cases
occurring after adult age, you should examine the
urine for albumen. This is highly important from
the point of view of prognosis, for whilst rheumatic
pericarditis generally ends in recovery, pericarditis
occurring with renal disease is generally fatal. The
disease may also develop in morbid conditions of the
blood as scurvy, and, though rarely, in the course of
scarlatina or variola.

Your previous examination will, in most cases, have
indicated that the pericardium contains some liquid
effusion ; but this is not invariable. Pericarditis, with
friction-sound, may occur, when the exudation is in-
appreciable (pericarditis sicca), or you may examine

* The results of the following observers approach very
closely and are probably nearest the truth : Fuller, 16 '7 ;
Duchek, 16 : Chambers, 18 per cent.

AUSCULTATION.

127

the case at a period when most of the effusion has
disappeared by absorption.

The importance of the observation of the sound of
pericardial friction is very great. This is one of the
very few great points that we have gained since the
time of Laennec. In most cases it is marvellous to
see how close and complete were the observations of
this great master. Our advances in physical diagnosis
since his day, until lately, have been neither great nor
rapid ; but in this case there is an exception. Laennec
sayS : — " There are few diseases more difficult to
recognize than pericarditis, or more variable in their
symptoms. ... I must acknowledge that mediate
auscultation does not afford much more certain signs
of pericarditis than the study of the general and local
symptoms." Thanks to the subsequent observations
of Stokes, Watson, and Bouillaud, we now know that
the existence and course of pericarditis can be traced
with precision as in the case of other cardiac diseases.

It is very rare indeed that a friction murmur fails
to be developed at some time during the evolution of
the pericarditis. It appears early in the disease.
Sometimes it disappears also early. Walshe has known
it appear and disappear within six hours. Sometimes
it appears, then disappears for a time during a period
of greater abundance of liquid effusion, then reap-
pears, to vanish gradually. Most frequently it lasts
for many days, varying in character and intensity, and
is heard over a less and less extended area as the
disease terminates.

The characteristics of the pericardial friction-sound
are chiefly — (1) Its quality; it is a "rubbing" or
" creaking " sound, resembling that produced by the
attrition of two surfaces of cloth or leather. It accom-

128

AUSCULTATION.

panies both movements of the ventricles, and is
admirably indicated by the expression of Sir Thomas
Watson — a " to-and-fro" sound. This rule is subject
to very rare exception when the rub is heard only
with the systole. We must postpone consideration of
this till we come to the differential diagnosis of val-
vular murmurs.

It is by no means uncommon to find tbat the rub of peri-
carditis has a triple rhythm. This was shown by the late Dr.
Hyde Salter to be due to the fact that roughening occurred
not only over the ventricles but over the auricles. The sound
over the auricles is presystolic, then follows the friction-sound
produced by the systole of the ventricles, and the third
portion is produced by the diastole of the ventricles.

(2) Its limitation. It is heard only over the superficial
cardiac region. This is very important. The sound is
not conveyed in certain directions from the heart-area,
as we shall find to be the case in regard to endocardial
murmurs. It is situated over the heart-muscle, and is
associated more with the movements than with the normal
sounds of the heart. At apex and base these normal
sounds may be heard— distant and feeble if there be
much effusion. On applying the stethoscope over the
intervening area occupied by the heart-muscle (chiefly
the right ventricle), the rubbing sound becomes mani-
fest Pericardial friction appears earliest, and most fre-
quently, at the base of the heart, near the great vessels.
(3) Its superficiality. It seems to be generated near
the ear If you withdraw your ear slightly from the
chest you may still hear the sound. Dr. King
Chambers calls attention to the following plan, as
affording valuable evidence :— Having observed the
sound with the ear, as usual, close to the stethoscope,
e-radually withdraw your ear, the stethoscope remain-
ing applied to the chest, the sound of pericardial

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friction will still, with great probability, be recogniz-
able. This nearness of sound to the surface is valuable
in the differential diagnosis between exocardial and
endocardial murmurs.

The friction- sound, however, may be very slight
and faint. In such case you should make your patient
change posture j the friction may then become more
manifest. The intensity may be increased by a change
from the vertical to the recumbent position, or vice
versa, or by inclining the body backwards or forwards.
In some cases a friction murmur is only heard when
a particular position is assumed by the patient. When,
therefore, your examination has led you to suspect
pericarditis, especially when you are satisfied that
there is effusion into the pericardial sac, and you are
anxious to discover evidence that the exudation is
fibrinous and tending to absorption, you should care-
fully auscultate in various positions, and note the
presence or absence of friction- sound.

Attention to the points I have mentioned will
generally enable you to recognize the existence of a
pericardial friction-sound ; but there is one condition
in which the diagnosis may be difficult. This is when
the friction is produced, not within the pericardial
sac, but outside, in the pleura.

You will remember the rule I adduced — to examine
carefully for disease in the left side of the chest. Sup-
pose that your examination has led you to conclude
that there is pleurisy with effusion, or pneumonia, or
that the lung abutting on the heart-region has under-
gone any of the changes occurring in the course of
pulmonary phthisis. If, in such conditions, you hear
a "to-and-fro" sound over the praecordium, remember
that this may be a pleural friction, modified by the

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movements of the neighbouring heart, and so made to
resemble the pericardial rub. The pleural surface
may be locally roughened by recent exudation, or
thickened by more remote, or by progressive inflam-
matory changes. If you have such a sound under
such conditions, and there is no other evidence of the
existence of pericarditis, the balance of probability
will be in favour of its exocardial origin. To further
the differential diagnosis, observe whether the sound
varies in character, and what are its relations with the
rhythm of respiration. Does it alter in intensity in
an irregular manner ? Does it become imperceptible
in some of the cardiac revolutions ? Is it more pro-
nounced at the end of a full inspiration 1 Observation
of these points will help you to a correct conclusion.

A pericardial friction-sound is less liable to varia-
tion than a pleuro-pericardial : the latter is most
evident when the lung is inflated, and thus the rough
pleural surface more closely adapted to the peri-
cardium, whilst the pericardial sound is most pro-
nounced when the heart is least covered by lung — that
is to say, at the end of expiration.

Having excluded the sounds which take their
origin in the structures superficial to the heart, we
come now to a wide field of inquiry— that which
includes the morbid sounds intrinsic to a diseased
heart. The subdivision of abnormal sounds which we
now consider is that wherein :

(2.) Abnormal sounds, occurring with or replacing
the normal sounds are heard only, or with a maximum
intensity, over the various situations of the valves,
or in definite relation with such situations.

You have applied your stethoscope over the aortic
cartilage (the point where the second right costal

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131

cartilage joins the sternum), and you hear a soft
blowing- sound j placing the tip of your finger over
the apex of the heart, or over the carotid artery, you
are convinced that the murmur coincides in time with
the pulse — that is to say, with the first sound of the
heart. Moving your stethoscope so as to auscultate
in a direction upwards beneath the right clavicle or
downwards over the heart, you find that the sound is
lost. It is, in fact, a first sound murmur localized over
the situation of the aortie valves, and it indicates an
alteration of the segments of these valves or a change
in the normal aortic orifice : the form and nature of
such change we shall consider presently.

Suppose, however, that you are satisfied that whilst
the sound which I have just mentioned is not propagated
downwards towards the heart, it is conveyed in a line
extending towards the right clavicle. This may possibly
be due to an aneurism of the ascending part of the
arch of the aorta, or of the innominate artery. To
establish or eliminate this hypothesis, you must
examine carefully for the concurrent signs of such
condition — a local prominence, pulsatory to the touch,
and perhaps communicating a thrill, a localized area
of dulness over the affected vessel, signs of alteration
of circulation in the distal branches of the diseased
vessel, and effects of the progressive pressure on
neighbouring structures, caused by the growth of the
aneurismal tumour.

You must remember, however, that whilst the
occurrence of aneurism may explain the existence of
the murmur, the hearing of this murmur is by no
means necessary to establish the existence of aneurism.
A systolic murmur is absent in a large number of
cases of aneurism.

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Aneurism eliminated, you have next to consider
whether the murmur may be ancemic. Here let me
say that you may find the differentia] diagnosis not
at all easy. Carrying- your stethoscope in the direc-
tion of the right subclavian artery, the right carotid,
the left subclavian and the left carotid, note the points
where the murmur disappears, and, if this happens,
where it reappears. In the great majority of cases
an ansemic murmur is a soft murmur ; it is heard in
the course of the great arterial vessels, not with
a diminishing" intensity, as one recedes from the
heart, but often with reinforcement over the arteries ;
a slight increase of pressure made by the stethoscope
increases the loudness of the murmur or develops it
when it is not heard. There is one observation which
will give you positive aid in the differentiation.
Having caused your patient to turn the head towards
the left, apply your stethoscope above the right
clavicle in the hollow behind the sterno-cleido-mastoid
muscle : you may now hear a continuous musical
hum, the origin of which is in the great veins. You
can at once distinguish it from the murmur which
you have just heard in the arteries, because, whilst
the latter is systolic, occurring only with the
arterial pulse, the former is an uninterrupted sound, a
sound called by French observers the bruit de diable,
"humming-top sound." By making pressure with
the finger over the veins above the stethoscope, the
murmur will be made to cease — a sufficient proof of
its venous origin. You should auscultate in like
manner on the left side of the neck. If you hear the
venous hum in either or both of these situations, you
have strong evidence that the murmur which you
have heard at the base and up the vessels is a so-called

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hceinic or anaemic murmur. But you obtain very
valuable collateral evidence from the general condition
of your patient. If there are the pallor and usual
signs of anaemia; if your patient is a female of an
age when the catamenia are commencing', or of a
later age, when there are troubles due to excess or
deficiency of the menstrual function or leucorrhcea, or
of a still later age, when there has been much loss of
blood — or if the case is one of a male, who has
suffered from hemorrhage or some potent debilitating
cause, or presents the signs of early phthisis, the
probability of the murmur being anaemic is rendered
very great.* I have seen it stated that anaemic
murmurs are seldom or never met with in young
children. I can only say, that at the North-Eastern
Hospital for Children, where we do not admit patients
above the age of twelve years, I have had many
opportunities of demonstrating this form of murmur.

' ' Cardiac murmurs of hamic origin are invariably basic,
they are loudest at niidstermim or in the anatomical site of
the orifices of the aorta and pulmonary artery. With this
point as centre they have a diffusion area of three to four

* I rind, from notes taken by myself, of 57 cases under my
own care where I discovered uncomplicated ansemic murmurs,
that 15 only were males. The ages were, under sixteen,
7 cases ; from sixteen to twenty-four, 18 cases ; from twenty-
four to thirty-two, 15 cases ; from thirty-two to forty, 6 cases ;
from forty to sixty-six, 4 cases. The arterial anasmic bruit
was heard at the base as well as in the carotids and subclavian^
of both sides, in 8 cases ; in both carotids in 11 cases ; in left
carotid and subclavian, in 6 cases ; in right carotid and sub-
clavian, in 4 cases ; in right carotid only, 1 case ; in both sub-
clavian, 2 cases ; in left subclavian, 6 cases ; at limited area
over base not propagated up vessels, 16 cases.

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inches in diameter, according to the intensity of the murmur
and the conducting qualities of the chest-wall; but they
never exhibit a definite line of propagation, as is the case with
organic murmurs in this situation." — Hayden, "Diseases of
Heart and Aorta," p. 252.

These murmurs, according to Guttmann, occur most fre-
quently at the pulmonary orifice, and very seldom at the
aortic.

I have said that you may find difficulties in deter-
mining whether a murmur he inorganic — i.e., haemic,
due to the causes just considered ; or organic — i.e.,
due to structural change of the aortic valves. This
difficulty occurs especially when the murmur is local-
ized at the aortic cartilage, and when, as is some-
times the case, a general condition of anaemia develops
or reinforces a murmur, due to structural disease.
We shall lessen the difficulty when we have contrasted
the organic with the inorganic hasic murmur.

In the case of the soft murmur, which we are still
considering- (for we shall hereafter notice the loud
basic murmur), the difficulties in diagnosing between
the anaemic and the structural may be great.

T have occasionally found murmurs in anaemic subjects
closely to resemble a double aortic — i. e, systolic and diastolic.
In such cases you will find that the systolic is the heemic
souffle heard at the aortic base, and generated either in the
aorta, the subclavian artery, or in the pulmonary artery ; and
the seeming diastolic is really a continuous venous hum
generated in the great veins of the neck. This continuous
hum is overpowered during the systolic period by the arterial
murmur, but it is audible during the diastole : — so the murmur
appears to be to and fro.

The cases wherein the chances are in favour of its
being structural will be, as I consider, in two classes
— one in young subjects, where there has been a his-

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135

tory of rheumatism, and especially where there is, or
has heen, chorea ; the other in patients past middle
life, where there is a probability of atheroma. In
these cases there may be but slight impediment to the
onward course of the blood in the aorta. It is very
seldom tbat the aortic valve is much affected by the
ordinary form of rheumatic endocarditis without the
mitral valve being- affected first or coincidentally.
Bear in mind that we are now considering a soft
murmur, heard alone over the aortic valves, without
discoverable alteration of the other valves. There is
a condition of the aortic valve in which the edges of
its segments are fringed by little villosities, so-called
vegetations ; these may give rise to a very soft aortic
murmur with the first sound. This condition is not
necessarily an accompaniment of rheumatism, but
where a valve is diseased by rheumatism or by athe-
roma, it is more apt to occur. In chorea, as we shall
consider hereafter, the vegetations are more fre-
quently found fringing the mitral valve, but they do
occur on the aortic segments. In patients after
middle life, such vegetations may be detached from
the valve by the force of the current of blood, and
being carried into the arteries, may plug one of the
arterial branches. Such may occur in various parts
of the system, but especially in the brain. Occurring
in the small terminal arteries of certain parts of the
brain, it is considered with great probability to be
often the cause of chorea ; when blocking a larger
trunk, it causes various forms of paralysis, or attacks
which are ascribed to apoplexy. Remember, there-
fore, the possibility of arterial embolism when you
hear a soft murmur localized at the aortic cartilage
in cases at the predisposing ages I have just alluded

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to, and wherein you do not find antenna to be a direct
explanation of the phenomenon.

So also you may turn the argument round and con-
clude that when, with these predispositions and under
these circumstances you hear a soft first sound murmur
localized over the aortic cartilage, such murmur is
probably due to a slight obstruction of the aortic
orifice, and that vegetations may fringe the valves.

We will now suppose that instead of the soft
murmur we have been considering, there is a loud
bruit heard over a wide area, hut having its maximum in-
tensity over the aortic cartilage. When you commence
to auscultate the heart region, you are at once cogni-
zant of a loud rough systolic murmur ; over the
second right costal cartilage this is very intense ; as
the stethoscope is carried towards the apex, the sound
is found to become less loud, and probably at the apex
itself it ceases to be audible. On auscultating in the
reverse direction the bruit is loudly heard in the
direction of the aorta and the carotid arteries. In
some cases it may be heard at the back, but then only
about the level of the spines of the scapula?.

Flint considers that an aortic systolic murmur is loudest at
the second right intercostal space close to the sternum.
Hayden considers that its maximum is at midsternum ;
exceptionally it is audible at the back in the left interscapular
space. Guttmann says that it is essential "in investigating
any case of aortic disease, that the whole of the sternum
should be carefully auscultated, as the murmur presents its
greatest intensity sometimes at one spot, sometimes at
another, on the surface of the bone." — " Physical Diagnosis,"
Sydenham Society's Translation, p. 291.

In case of a murmur having these characters, if you
have eliminated the probability of an ansemic causation,

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137

you will have no difficulty in diagnosing- obstruction
(stenosis) of the aortic outlet due to a diseased condition
of the valves. The concurrent signs willbe hypertrophy,
without dilatation, of the left ventricle, with small
hard arterial pulse. The pathological changes which
give rise to this form of murmur consist in thickening,
rigidity, and fusion of the segments of the semilunar
valves of the aorta, so that the orifice of exit of the
blood from the left ventricle is narrowed. This may
occur to such extent that the orifice will barely admit
a probe. Sometimes the valves are hardened from
atheroma and calcareous deposit, sometimes fringed
and obstructed by fibrinous vegetations or warty
excrescences, sometimes roughened by ulceration.

It is important, even from a diagnostic point of view,
to attempt to define under what conditions these
various causes of obstruction of the aortic orifice
arise. A significant and somewhat strange argument
meets us at the very commencement of the investiga-
tion. Taking the positive evidence of post-mortem
examinations, lesions affecting the aortic valves alone
are of very common occurrence. Dr. King Chambers,
in analysing 367 cases in which valvular lesions of the
heart were discovered at the autopsies, found that the
aortic valves were solely affected in 107, the mitral only
in ninety-six. The general experience of observers
has been that the frequency of disease in the mitral
valve alone, and at the aortic orifice alone respectively,
is about equal, but that the proneness of the mitral
is slightly the greater. Compare this observation
with clinical experience ; I think you will find all
physicians concur in saying that mitral lesions per se
are diagnosed far more frequently than aortic. Of
the hundred cases of heart disease which I mentioned

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in an early part of these Lectures, as observed by
myself, only fifteen were declared by the physical
signs to be solely due to morbid changes at the aortic
orifice, whilst no less than fifty-eight were mitral. It
seems fair to conclude from these facts that aortic
lesions are often present during life, but are only dis-
covered after death. The regurgitant lesions which
we shall soon consider, are much more baneful in their
obvious effects than the obstructive lesions of the
aortic valves. It is very probable, therefore, that
obstructive lesions are more frequently present than
detected. Positive experience confirms this view in
many cases, especially of sudden and alarming symp-
toms in old people with cerebral or visceral disease ;
patients who are sometimes brought moribund to the
hospital are found to present obstruction of the aortic
outlet. Now as to the forms of disease which pro-
duce aortic obstruction. Of twenty-four cases ob-
served by myself in which the physical signs indicated
aortic obstruction, ten were obviously rheumatic,
nearly all having suffered well-defined rheumatic
fever. Flint records that of thirty cases of aortic
lesions, rheumatism had occurred in sixteen. We
shall see, however, that the aortic valves are less
prone to be attacked by rheumatic endocarditis than
the mitral. Rheumatic endocarditis attacks first the
mitral valve, then extends upwards involving the
endocardium lining the ventricle, till it includes the
aortic valves in the morbid change. In the majority
of cases in which we hear an aortic obstructive
murmur without evidence of impairment of the mitral
valve, endocarditis has not been limited to the aortic
valves, but has begun in the mitral, though its effects
have not been sufficient to destroy the integrity of
the latter.

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139

Besides the alteration of the valves from rheumatic
endocarditis, there is another cause which is very
common in inducing- obstruction — atheroma. In this
the valves are often incrusted with calcareous deposit.
This form of alteration is exclusively met with after
middle age, and is by far the most common cause of
aortic obstruction in patients past the prime of life.

The most common cause of mechanical impediment at the
aortic orifice is not primary disease of the heart or of its valves,
but of the aorta adjacent to the valves. The latter become
implicated by extension of the disease. The morbid process
(aortitis; endarteritis) commences by swellings, localized in
patches, in tbe internal coat of the vessel, with infiltration of
the layer next to the endothelium by cellular elements ; sub-
sequently such infiltration extends outwards to the muscular
coat. In the later stages degeneration occurs, so that the
elements become yellowish and softened from fatty change, or
undergo calcareous transformation, giving rise to hard stony
plates in the wall of the vessel. This stage of degeneration,
fatty or calcareous, is the condition known as atheroma.
Occurring in the neighbourhood of the aortic semilunar valves,
these are involved in the thickening ; so they may become of
fibro-cartilaginous consistence, or hard and bony from calcareous
transformation. The conditions leading up to such morbid
change in the arteries are probably (a) alcoholism. Dr. Hay-
den believes that amongst the humble classes alcoholism is the
chief cause of the diseases of the aortic valves — that is, it
induces the lesion of the aorta, which involves the valves; (b)
gout or the lithic acid diathesis. This, according to the same
authority, is the most frequent disposing cause amongst the
rich. The acute and sub-acute forms of rheumatism do not
predispose to the affection, whilst the gouty forms, such as
chronic rheumatic arthritis, are distinctly associated with the
arterial disease ; (c) syphilis. I have had abundant evidence, to
my mind conclusive, that endarteritis and aortitis can be the
direct result of the action of the syphilitic poison ; (d) muscular
strain. This has been strongly insisted upon by Dr. Clifford
Allbutt, who has pointed out the proclivity to aortic disease of
persons whose avocations subject them to severe or sustained

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effort, such as soldiers, strikers, lifters, &c. I confess I am not
convinced that mere muscular effort can induce the disease in
^previously healthy aorta. In the cases I have observed, when the
affection existed in the classes mentioned by Dr. Allbutt, there
has been a strong suspicion that a concurring cause might have
been alcohol or syphilis, or both combiued. At all events, effort
is a proximate cause, and with it may be classed constriction
of the chest by tight clothing, &c. ; (e) a condition of per-
sistently high tension in the general arterial system. This is
most typically expressed in chronic renal disease, where there
are tight arteries and hypertrophy of the left ventricle. I
entirely agree with Dr. F. A. Mahomed, who has called
attention to the fact that this tendency to high arterial tension,
may be manifested in the early ages of life, and when there is
no renal implication whatever. It is, therefore, of the highest
practical importance to recognize it, to caution the subjects of
it against any possible overstrain, and so to ward off the
actual disease of the arterial coats, to which it tends. In these
cases the pulse may be recognized as hard and full by the finger,
and there may be signs of some hypertrophy of the left
ventricle, with heightened tension in the aorta, as shown by
accentuation of the aortic second sound ; but there is no
evidence comparable in value with that obtained by the
sphygmograph (see Part II.) If at any age a condition
of high tension in the arteries is demonstrated, the danger
of disease in the arterial coats should be recognized.

For the differential diagnosis of the rheumatic and the
atheromatous forms of disease occasioning obstruction at the
aortic outlet, the evidence afforded by the sphygmograph is of
great value. The tension in the atheromatous form is much
greater than that which iisually obtains in the rheumatic ; in
the former is foimd the typical trace of aortic obstruction.
See typical tracing of aortic obstruction in Part II.

By both these forms of disease (rheumatic endo-
carditis and atheroma) the narrowing of the aortic
orifice may be extreme, and yet the signs of subjective
and objective may not be pronounced. In two cases,
one mentioned by Stokes and another occurring' in

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141

America, the orifice left in the fused and hardened
valves was so small as only to admit a small probe,
and yet disease of the heart was not suspected till the
occurrence of acute disease of the lungs which proved
fatal. If the signs in such extreme obstructions are
obscure, they are still more so in the form of endo-
carditis characterized only by vegetations upon the
valves. According to French observers, these lesions
have nothing to do with rheumatism, but are associ-
ated with various maladies (Lancereaux, " Anatomie
Pathologique," p. 220). It is this form of endocarditis
which is especially associated with chorea in young
subjects, and with the accidents of cerebral embolism
in the old. There is yet much obscurity as to its '
patbogenesis ; it is characterized by hyperplasia of the
superficial layer of the endocardium, giving rise to
little excrescences forming groups upon the ventri-
cular surface of the valves, sometimes fringing their
free borders. These vegetations are often attached
to the surface of the valve by slender pedicles
easily detached ; their size is frequently augmented
by the attachment of fibrine derived from the blood
current. It differs in histological characters from the
rheumatic form of endocarditis which affects the deeper
fibrous structures of the valves and involves their
whole substance. It seems very probable that the
French observers are correct in differentiating this
form pathogenetically. Lancereaux says that it may
occur under various obscure conditions, but especially
in alcoholism, the puerperal state, and, perhaps in
intermittent fever. Whether isolable or not, we must
admit that this form of endocarditis may accompany
other forms — in fact that, though it may probably
arise per sc in certain as yet untraced conditions, it

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frequently occurs upon any valve which has under-
gone morbid change from other causes.

Another form of disease affecting the aortic valves,
which, though rare, must be borne in mind as affecting
diagnosis, is that in which the valves are ulcerated.
Under certain circumstances of depressed vitality, the
valve already diseased tends to ulcerate ; the patient
is seized with rigors and symptoms of septic poison-
ing. The debris of the ulcerated portions of the
valves form plugs which, being carried by the current
of blood, cause embolism of many arteries through-
out the system as well as general blood-poisoning.
In eleven cases recorded by M.. Lancereaux, the aortic
' valves alone were affected by the ulceration in six.
The disease may arise in various adynamic conditions ;
several cases have been recorded as occurring in the
puerperal state. You may conclude that when in a
case of aortic obstructive disease (mitral conditions we
shall consider hereafter) your patient is seized with
severe rigors, with pysemic symptoms, with vomiting
and diarrhoea, with alternations of very high with low
temperatures, and especially with signs of cerebral
embolism, there is present an ulcerative endocarditis.
The disease is uniformly fatal.

To resume, concerning aortic obstructions in ge-
neral, especially as regards prognosis. "When you have
a loud obstructive murmur with a history of rheu-
matism or of senile change, with some cardiac hyper-
trophy, the lesion, compensated as it is by increased
force of the heart, need not give occasion to a grave
prognosis. The patient may with considerable proba-
bility live long in spite of the obstruction. In the
case of the soft murmur you should be guarded in
your prognosis. Examine your patient with great

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143

care, for these cases are often overlooked. Remember
in children the proclivity to chorea ; in advanced age,
in puerperal conditions, in alcoholism, and in Bright' s
disease, the danger of embolism. When you are called
to a case of so-called apoplexy where the symptoms
occur very suddenly, always carefully auscultate the
heart, remembering- the great probability that there
has been cerebral embolism by detachment of a vege-
tation from a diseased valve.

We return now to the aortic cartilage. Suppose
that we find the first sound to be unaccompanied by
murmur but not so the second or diastolic sound.
The latter, wbich should consist only of the click occa-
sioned by the closure of the semilunar valves, is com-
plicated by a murmur. Like the systolic, which we
have just considered, this may be soft and short, or
loud and pronounced. If soft, you will notice first,
its point of greatest intensity. You will probably
hear it at the aortic cartilage, but on carrying your
stethoscope to the left side of the sternum and auscul-
tating over the cartilage of the third or fourth rib, it
will be yet louder. The reason of this we shall pre-
sently see. Notice in the next place whether some of
the clicking sound of the closure of the aortic semilunar
valves is heard with it— i.e., whether it accompanies
and not replaces the aortic second sound ; if this occurs,
it is evideuje that some of the segments of the valve
are capable of performing their functions— that the
lesion does not involve them all.

This second sound murmur, instead of being soft
and local, may be loud and prolonged ; in quality it
may be rough, or musical, and it may be heard over
a wide area. You may not hear it over the right or
left base, or up the great vessels, but by carrying

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your stethoscope downwards along- the centre-line of
the sternum you arrive at a spot where the murmur
with the second sound is distinctly heard. Excep-
tionally it is heard only as you get near the apex of the
heart. You have many collateral signs to guide you
in the diagnosis : the visible throbbing of the arteries,
the heaving of the praecordial region, the signs of
hypertrophy and dilatation of the left ventricle. In
no condition is the probability greater of enlargement
of the heart ; in some cases there is enormous increase
of mass and weight, the so-called " cor bovinum."

There is another objective sign which I take to be
of great value. On making' an ophthalmoscopic examina-
tion of the retinal vessels by means of the erect image,
you observe pulsation of the veins or arteries, or of ooth.
Dr. Stephen Mackenzie has done great service in
drawing attention to this sign. I have made ophthal-
moscopic examinations in a large number of cases in
which an aortic second sound murmur existed, and I
I have rarely failed to find visible pulsation of
the retinal vessels. Such pulsation is found most
commonly in the veins, but both arteries and veins
pulsate in many cases. This sign may have great
value, especially when other signs are masked — for
example, when the lungs are affected, and the loud
rhonchi and rales of bronchitis render it difficult to
hear the sounds of the heart.

Suppose that you have heard a second sound
murmur, and that by its position and by the existence
of collateral signs you have located its production in
the aortic outlet, what is its pathological significance ?
It means that there is regurgitation of the blood-
stream into the left ventricle' when the heart is in
diastole, on account of the imperfect closure of the

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valves which guard the aortic outlet. In the case of
the systolic murmur, we had obstruction afforded to
the onward stream of blood through the aortic orifice ;
in the case of this diastolic murmur we have in-
sufficiency of the valves to close the orifice after the
systolic gush is over.

Imperfection of the valves, permitting regurgitation
into the left ventricle, is brought about by patho-
logical processes similar to those which induce
obstruction. In the rheumatic form of endocarditis
the valves, after having become thickened by hyper-
trophy of their connective tissue, undergo a slow and
gradual process of contraction, so that the free edges
of the valves are retracted from the centre, and a gap
of necessity results. Or, in the villous form of
endocarditis, a bunch of vegetations may depend
from the segments of the valve on their ventricular
aspect, and so weigh down such segments as to pre-
vent their apposition in diastole. These masses of
vegetations may vary in size from a pin's head to
a walnut. Again, such imperfection of the valves as
may induce regurgitation, may be caused by the
rigidity of segments which have undergone athero-
matous change. In rare cases the valves may be-
come ruptured through violence or perforated by
ulceration.

In all these pathological conditions, the mechanical
effect is reflux of blood, in diastole, through the
abnormal gap in the valves. The secondary effects
are, first, that there is a deficiency of supply of blood
to the general arterial system ; secondly, that the left
ventricle contains always too much blood. The
further consequences are, that the ventricle under-
goes compensatory hypertrophy, thus making up for

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the loss to general arterial system induced by the
reflux, and that, from its over-repletion (for you will
understand that it contains blood early in diastole
when it ought to be empty, and the normal amount
of aerated blood is superadded to the amount which
has regurgitated through the imperfectly-closed aortic
orifice) the ventricle becomes dilated. You will thus
comprehend why, in the case of aortic obstruction, we
have hypertrophy only of the left ventricle, whilst in
aortic regurgitation we have hypertrophy and dilata-
tion. In obstruction there is enhanced power of the
ventricle to overcome the difficulty, but no distension
of the ventricle by an abnormal content of blood.

You are now in a position to understand the
mechanism of the murmur of aortic regurg-itation — it
is the murmur caused by the backward rush of blood
through the partially-closed and imperfect aortic
orifice. Remember that this is not a merely passive
reflux — it is not simply by the weight of the column
of blood that the murmur is occasioned. The ven-
tricular systole drives the blood into arterial channels
which are both elastic and muscular. There is a
recoil, therefore, of all the arteries which have been
distended by the ventricular systole, and the blood is
forcibly urged backwards into the ventricle. Thus
you may understand how prolonged and loud the
murmur is in some cases.

Aortic regurgitation is most commonly met with at
or after the prime of life (of fifty cases noted by Von
Bamberger, only fifteen occurred before the age of
thirty), and in the male sex, the proportion in recorded
cases being three males to one female. The pro-
gnosis is generally bad ; in the rare cases of youthful
patients, compensation by hypertrophy of the ventricle

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147

may be such that but little trouble is experienced,*
but when adult life is attained the lesion is one of the
gravest tbat can affect the heart. This is one of the
conditions in which sudden death may occur, and the
subjects sbould be cautioned against excitement and
over-exertion.

Suppose, now, that you hear two sounds at the
aortic cartilage, the one with the systole and the other
in the diastole. There is a double murmur. Or over
certain spots whereto, as I have described, an obstruc-
tive " bruit" may be carried by conduction or convec-
tion, you may hear a first sound murmur, and over
other spots in the direction of the retrograde current
you may hear a second sound murmur. You may
conclude in such cases that there is a combination of
the two lesions which we have just considered — that
there is aortic obstruction as well as aortic regurgita-
tion. This is not uncommon. The semilunar valves,
roughened on their ventricular aspect, or rigid and
offering an obstructed orifice of exit for the blood, are
also imperfectly opposed in diastole.

We have now considered three forms of heart-
murmur — the aortic direct, or obstructive ; the hsemic
or ansemic, and the aortic regurgitant or murmur of
aortic insufficiency. It will be well to make a short
digression and endeavour to understand the physical
cause of these abnormal sounds.

There are few subjects which have been more
voluminously debated than the physical causes of
cardiac murmurs, and few concerning which there is
less accord. It would appear that each observer has
taken infinite pains to elaborately convey his impres-

* I have met with several instances of the affectiou in
children, who nevertheless evinced little or no cardiac distress.

L 2

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sions, with the result of convincing- no one hut him-
self. No two observers seem to he in complete
agreement. It will serve, I think, no good end to
make a critical examination of the various theories
which have heen propounded ; I purpose, therefore,
to express my own views on the subject in a way
which I conceive to be the most simple, the most
practically useful, and the most in accord with the
present teachings of science.

1. Sound is the effect of vibrations transmitted to
the organ of hearing. The sounds of the heart,
normal and morbid, are due to vibrations conveyed
from the surface of the thorax to the ear. If the ear
be applied closely to the chest (immediate ausculta-
tion), the vibrations of the thoracic wall are commu-
nicated to the intervening layer of air, and then to
the external ear. If the stethoscope be used (inter-
mediate auscultation), the vibrations are transmitted
to its walls, and by these to the air intervening
between the ear-piece and the tympanum. The tube
of the stethoscope does not perceptibly weaken the
sound. " The law tbat the intensity of sound
increases in inverse proportion to the square of tbe
distance, does not apply to the case of tubes, espe-
cially if they are straight and cylindrical."* Many
vibrations are communicated to the chest-wall, from
the movements of the heart, and the fluids and
structures in relation with it, which are not capable
of giving rise to impressions of sound. Such are im-
pulse and thrill. To be perceived by the auditory
centre, vibrations must have a certain rapidity and a
certain amplitude or intensity. The tactile faculty

* Ganot's " Elementary Physics," translated by Atkinson.
Eighth edition, p. 177. London : Longmans.

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149

can appreciate vibrations which are too slow for the
auditory, and the auditory those which are too rapid
for the tactile ; but the areas of perceptibility by the
two faculties overlap, so that vibrations may in some
cases be detected bv both and in others tactile im-

pressions may be supplementary in duration to audi-
tory or vice versd. Thrill may precede, accompany,
or succeed murmur. It is to the thoracic surface,
then, whereto vibrations are conducted, some of which
are sonorous, or capable of exciting- auditory percep-
tion. It is at the thoracic surface alone that the con-
ditions obtain for the production of sound, for it is
here only that the vibrations are given to the air.

2. The sounds heard are produced by vibrations
communicated to the air by the thoracic wall, irre-
spectively of the mechanical means by which such
vibrations are produced. This proposition is proved
by the telephone. By it sounds are not transmitted,
but vibrations similar to those of the sounds are pro-
duced, and the effect on the organ of hearing is the
same in the one case as in the other. It is further
demonstrated by the phonograph, by which sonorous
vibrations are made to record themselves as motion-
vibrations upon the surface of a soft metal ;
these being by mechanical means recommunicated
to the air, the original effect on the organ of
hearing is reproduced. There is synthesis of sound
from the mechanical vibrations. It appears to me,
therefore, that the qucestio vexata of the site and
mode of production of sounds in the heart, the vessels,
or the fluids, is a barren controversy. Sounds are
not produced, save at the thoracic wall, where the air
receives its undulations. In the heart and its sur-
roundings are produced vibrations, which at the sur-

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face may, or may not, give rise to impressions of
sound.

3. The normal sounds of the heart partake rather
of the character of noise than of music ; they are
either sudden and abrupt, or dull and muffled.
The second sound is the uncomplicated sound of
valve-tension, such as one imitates by suddenly
stretching- a previously lax piece of membrane. The
sound is of too short a duration to be capable of
musical determination ; the auditory faculty receives
it as a shock. The first sound is for the most part
similar to the second — that is, it is chiefly due to
valve-tension occurring over a larger area (in propor-
tion, as the mitral and tricuspid valves combined
exceed in extent the aortic and pulmonary), but mo-
dified first, because the intervening walls of the
ventricles subdue the sound in proportion to their
thickness • secondly, because the (muscular) sound of
the contracting ventricles supplements and pro-
longs the valve-sound. The muscular sound is dull,
because the fibres mutually interfere to arrest their
own vibrations.

4. The morbid sounds which are heard in relation
with the heart and vessels, partake, on the other hand,
rather of the character of music than of noise. They
are not abrupt, but, varying in intensity and pitch,
commence at one end of the scale as a scarcely per-
ceptible blowing (aspirate), and become rough and
grating, or else occur in many varieties of pitch up
to the production of a distinct musical note.

5. The organic conditions giving rise to such mur-
murs as have their origin in disease or abnormality
of the valves or orifices of the heart may be for the
most part referred to two types : first, in which the
orifice which originates the vibrations occasioning the

AUSCULTATION.

murmur is converted into a ring ; secondly, in which
across the orifice and in the blood-stream there is a
vibrating- tongue. In these conditions a strict analogy
obtains with musical instruments. In one case the
fluid which is the intermediate agent of vibration is
the blood, in the other it is air. The first type is
exemplified by the flute, the cornet, or other usual
form of wind instrument ■ in these, vibrations are pro-
duced by the forcing of air, under compression,
against the wooden or metallic walls of the instru-
ment. More familiarly still, it is illustrated by
whistling produced by the mouth with the lips pursed
up so as to make a circular aperture, the pitch of
the note produced being heightened in propor-
tion to the decrease in size of the aperture, and
the intensity or loudness varying in proportion to
the force of expiration. It seems to me a popular
error to ascribe too much of the sound-producing
agency to currents of air forced through the aper-
ture. The air is rather the intermediate than the
immediate agent — that is, the force of expiration
sets the solid boundaries of the orifice vibrating,
these vibrating solids communicate their vibrations to
the air, and the stream which issues from the orifice
has little to do with the production of sound-vibra-
tions. This can be easily proved. Produce with the
mouth an audible " whistle," then apply the fingers
to the pursed-up lips so as to stop their vibrations,
but in such manner that the exit of air from the
orifice is unimpeded. You will find that though the
air issues just as before, the " whistling " sound is
arrested by the arrest of vibration of the walls of the
orifice of exit. A similar experiment with a metallic
whistle has the same result. So I think we may infer
that the vibrations which give rise to sound in the

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case of the intra-cardiac murmur start from the solid
structures rather than from the fluid blood, though
this latter is an agent for the communication of vibra-
tions to the solid structures. Savart's fluid veins are
agents for the production and communication of
vibrations, which imparted to solids give rise ulti-
mately to sonorous vibrations. The second type of
murmur is illustrated by the Jew's harp or accordion,
in which a tongue of metal is set in vibration. At
the aortic orifice it is exemplified when a shred of
fibrin, a prolongation of fibro-cartilaginous material
or the debris of a ruptured valve stretches across and
vibrates in the blood-stream. When so orio-inatinsr,
the murmur often has a markedly musical quality ; it
usually is diastolic, but may be systolic, and is not
unfrequently double.

5. We have already seen (p. 96) that the sounds
heard over the heart-region are not immediately
superficial to the positions whence they originate —
that is, the vibrations which give rise to sonorous
impressions are conveyed from their sources to cer-
tain areas of the thoracic surface. Such transmission
occurs in two modes (1) by condtiction, so termed
when the vibrations are conveyed by still media or
solid structures. The normal lung, filled as it is with
air, is a very bad conductor of vibrations ; when,
however, there are condensations of the pulmonary
tissue, exudations or solid growths, these may act
the part of conductors, and the heart sounds, normal
or abnormal, may be heard in unusual situations. In
the case of the diastolic aortic murmur, the sternum,
which is comparatively a good conductor, causes the
sound to be heard in a direction down its central-
line or along its left border. (2) There is, however,

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153

another way by which, vibrations are transmitted,
that is, by media in motion. A murmur is best
heard in the direction of the current of blood. This
was called by the late Dr. Hyde Salter the law
of convection of murmurs, and explains away many
difficulties. This also may be illustrated by analogy
with the air. On a still day everything- may be
silent, but let a breeze spring up, and the sounds
— of distant bells, for instance — are wafted to the
ear. The sound is heard only in the direction of
the current of air ; if the wind change it will be no
longer audible. In like manner, a cardiac murmur
is heard in the direction of the current of blood. In
the murmur of aortic obstruction, the vibrations gene-
rated at the time of the systole are carried by the
blood-stream into the aorta and up the great vessels.
In the murmur of aortic regurgitation, the direction
of the current of blood at the time of occurrence of
the sound is exactly the reverse of the former ; the
stream is gushing back into the left ventricle, and
the line of convection is downwards from the aortic
cartilage to the apex of the heart. In some excep-
tional cases the regurgitant murmur is only heard at
or near the apex.

The late Dr. Hyde Salter called attention to the fact that a dias-
tolic murmur generated at the aortic outlet was in exceptional
cases audible only at the apex of the heart. Two illustrative cases
were quoted {Lancet, August 14,1869, p. 225). In one ofthese there
had been, no doubt, rheumatic endocarditis : — "It was quite
certain that the murmur so plain at the apex and inaudible at
the base, was due to aortic regurgitation — that is, that the
stream of blood flowing down towards the apex carried thither
the sonorous vibrations of which conduction failed to give any
evidence in the immediate neighbourhood of their production."
In the second case there was " a very distinct diastolic mur-

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mur ' heard at the left apex in the case of a female in whom it
was extremely probable that there had been rupture of the
aortic valves. These observations have been confirmed, ampli-
fied, and rendered of great practical importance by Dr. Baltha-
zar Foster (see "Clinical Medicine," p. 112 et seq. London,
Churchill, 1874). Dr. Foster's observations were also in cases
of rupture of the aortic valves, and the experience of one case
dictated a precise diagnosis in another. When a diastolic
murmur of aortic origin is conducted to the left apex, "it
depends on the regurgitation taking place through incom-
petency of the posterior aortic segment , either at its right angle
or through perforation of its curtain." In such pathological
conditions the regurgitant blood-column falls upon the upper
segment of the mitral valve ; this was proved, not only by ex-
periment after death, but by inference from the thickening of
the segment which had probably taken place on account of the
stream which had been projected against it during life. The
vibration produced, notwithstanding that the lesion is aortic,
being of the mitral valve, is heard in the mitral area— that is,
at the apex. Dr. B. Foster adds :— "I believe we may also
say that a similar murmur propagated towards the ensiform
cartilage indicates incompetency of either the left or the right
coronary segment, by which the regurgitant current is thrown
more upon the septum of the ventricles."

The diagnosis of rupture which may occur in the case of
previously healthy aortic valves is to be made from the history
of the onset of symptoms :— sudden pain at the prsecordium,
palpitation and dyspnoea arising in direct relation with violent
strain, effort, or after a blow upon the sternum, in the absence
of a history of rheumatism, but attended with the physical
signs of aortic regurgitation, or of aortic obstruction and
regurgitation combined. Dr. Hayden adduces also the exist-
ence of systolic arterial thrill as an important sign for the
physical diagnosis of such cases.

Supposing Dr. Foster's experience to be confirmed, it becomes
possible to determine in cases of aortic regurgitation which seg-
ment is affected, and this may be of high importance as regards
prognosis. " Two of the segments have above them each
a coronary artery which is filled by the blood-column as it
rebounds from their curtains. When these segments are torn
down and retroverted, the regurgitant blood-column running

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155

past the mouths of the coronary vessels must to some extent
diminish the amount of diastolic blood- wave which they receive,
and consequently impair the heart-nutrition. . . . That seg-
ment of the aortic valves by whose incompetency, we believe,
a murmur is specially carried to the left apex, has no coronary
artery above it, and therefore when it is affected, we should
expect the coronary circulation to suffer less than when either
of the other segments is imperfect." Death usually follows
rupture of the aortic valves within three months, the maximum
duration of life has been four years and a half. In the case of
injury to the non-coronary segment recorded by Dr. Foster,
life was prolonged to nearly three months ; whilst the duration
was eighteen months, and three months in the other cases. It
would appear, therefore, that when in a case of aortic regurgi-
tation a diastolic murmur is localized at the apex of the heart,
it is probable that the posterior segment of the aortic valve is
affected, and that the chances of duration of life are greater
than when the murmur is heard at the usual situation over
the sternum.

6. Vascular murmurs — the so-called hasmic mur-
murs— are due to vibrations produced in the walls of
vessels. The murmur heard over the site of the
aortic valves is the effect of vibration of the initial
portion of the aorta; sounds of similar character
heard over the carotid and subclavian arteries are due
to vibrations of the arterial walls occurring- in cer-
tain areas. It is characteristic of these murmurs
that they are not transmitted along- the vessel in un-
broken continuity, but are heard over certain portions
of it ; they are much intensified by a little pressure
with the stethoscope. Murmurs closely resembling-
these may be produced by such pressure even in con-
ditions of health. Vascular murmurs may be heard
in acute febrile diseases, but they are especially asso-
ciated with anaemia and chlorosis. It has been proved,
both by Marshall Hall and by Hope, that such
murmurs can be induced in animals by copious bleed-

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ing-s, and we are familiar with the fact that they
appear in the human subject after sudden and copious
haemorrhage. That they are not due to the mere ab-
straction of quantity of blood, however, is proved by
the experiments of Richardson, who found that the
" bruits " were produced in dogs after injection of
large quantities of water into the veins. Moreover,
in common with other observers, I have noted them
in cases where there was good volume of blood in
the arteries. There can be little doubt that a watery
condition of the blood aids to the production of such
murmurs ; and this is only probable, for a mobile
fluid can oscillate much more readily than a viscid
one. Neither decrease in quantity nor deterioration
of quality in the blood can, however, be the only and
absolute cause of the murmur, for the latter is not
constant in conditions of antemia, nor is it heard
throughout the great arterial vessels. The localiza-
tion of the murmur points to a local cause, and this
cause I take to be a modification of tension in the
arteries in certain areas, whereby the walls of the
artery in these portions are rendered prone to vibrate.
These murmurs are particularly marked when there
is any cause for the abnormal conduction of vibrations
to the surface of the chest. This is especially the
case in subclavian murmur, which is thus of dia-
gnostic importance in the early stages of disease in
the apices of the lungs. The venous hum — bruit de
diable — has its origin in the internal jugular vein. It
is due to the vibration of the coats and valves of the
vein, just as the arterial murmur is due to the vibra-
tion of the walls of the artery, such vibration being
communicated by the whirling movement of the
blood. " The blood flows from the relatively narrow

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157

jugular vein into the relatively wide bulb (the part at
which the vessel debouches into the innominate vein),
and is thus caused to sweep in a somewhat spiral
course round the walls of the chamber, so that the
mode of origination of the venous hum may be re-
garded as strictly analogous to that of murmurs in
the arteries. This dilatation at the end of the vessel
remains permanently wider than the upper part of
the vein, as its sides are held apart by the tense cer-
vical fascia."* The venous hum is intensified when
the patient turns the head jrom the side which is
auscultated ; thus, the superficial structures of the
neck being put upon the stretch, the jugular vein is
compressed and narrowed. It is obscured or extin-
guished when the patient resumes the recumbent
position, the aid to the force of the current afforded
by gravity being thus removed. The hum is gene-
rally louder on the right side of the neck.

Chauveau and Corrigan have both demonstrated
experimentally that " when a liquid current is hurried
past a constriction in its passage into a wider space
b eyond, a ripple or perturbation in the current is
created, giving rise to vibration and murmur."f
This I consider to be the key to the explanation of
vascular murmurs, both venous and arterial, only I
do not attribute the sound-producing vibrations to
the liquids, but to the solids, to which the vor-
tiginous movements of the fluids impart motion. In
the case of the basic aortic murmur, there is a condi-
tion of impaired tension at the origin of the vessel,
so that its walls vibrate. In the case of arterial

* Guttmanu's " Handbook of Physical Diagnosis,'' p. 308.
t Haydea's " Diseases of Heart and Aorta," p. 250.

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murmurs there is non-equable tension of the vascular
wall, and at the portions where tension is impaired,
eddies are produced which set these portions vibrating-.
The venous hum is the effect of deficient impletion or
defective muscular tone in the jugular, whose walls
vibrate owing' to the eddies developed in its fluid
contents.

159

LECTURE VII.
AUSCULTATION.

PART III.

Hsemic pulmonary murmur— Pulmonary stenosis— Relation to
cyanosis — Tricuspid regurgitation— Ventricular murmurs-
Murmurs in chorea — Myocarditis — Arguments concerning
cause of non-valvular murmurs — Cardiac phenomena of
typhoid fever— Organic mitral murmurs— Causes of mitral
lesions— Varieties of lesion— Mitral insufficiency— Mitral
stenosis.

We now leave altogether the region of the aortic
valves and cross the sternum to the second left inter-
space and the sternal end of the third cartilage— the
area of the valves of the pulmonary artery.

Suppose that you hear a soft murmur with the first
sound localized in the pulmonic area. The chances
are enormously in favour of this being- inorganic-
vascular. Observe all the rules as regards differential
diagnosis which I have given you, for the discrimina-
tion of anemic murmurs when heard at the aortic
base. Especially notice whether the sound is carried
along the left subclavian. If it be strictly localized,
the haemic murmur may be generated in the pul-
monary artery. Dr. Flint considers that an inorganic
murmur emanates as frequently from the pulmonic
orifice as from the aortic. I must say that I have not
observed this in my own experience. I have found
the soft murmur heard at the left base in the
majority of cases, to be distinctly traceable to the left

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subclavian artery. I would say of a soft systolic
murmur localized in the pulmonary area, always
assume it to be inorganic or independent of structural
change, unless there is strong collateral evidence in
favour of its being organic.

Assuming that you have eliminated anaemia as a
possible explanation of the murmur, you have yet to
consider whether the sound may be produced by the
pressure of a tumour upon the trunk of the pulmonary
artery. It has been said that tuberculous lung can
give rise to such pressure. I should explain the mur-
mur heard in these cases as due to the conduction by
the tubercular consolidations of a hamric murmur
generated in the pulmonary artery. Tumours in the
mediastinum, enlarged bronchial glands, cancerous
and other growths in the lung may undoubtedly
cause pressure against the trunk of the pulmonary
artery, and give rise to a systolic murmur. All
such probabilities of extra-cardial causation you must
eliminate by careful examination.

We will imagine that you have eliminated anaemia
and pressure on the pulmonary artery as probable
causes, and yet you hear a localized murmur over the
situation of the pulmonary semilunar valves. This
murmur with the first sound may be soft, and heard
only at the spot indicated, or it may be loud, and
heard over a wide area, but distinctly most intense
about the third left cartilage. You may be sensible
that it is very superficial— generated very close to the
ear. A murmur with these characteristics will, with
much probability, be due to obstruction of the pulmonary
artery, but before completing the diagnosis we will
briefly consider the pathological causation and clinical
concomitants of such a condition.

AUSCULTATION. 161

In considering aortic disease, I made no mention of
congenital defects, because these so rarely affect the
aortic orifice that they do not practically influence
diagnosis. Aortic defects are not congenital, hut ac-
quired. It is quite otherwise with pulmonary lesions.
Intra-uterine malformations are far more likely to
involve the pulmonary artery; moreov.er, when
endocarditis attacks the "foetus in utero" it is the
right chambers of the heart that are much more fre-
quently affected. The rule in after-life is exactly
reversed.

The pathological causes which give rise to obstruc-
tion of the pulmonary orifice operate chiefly in foetal
life. Through faulty development, the pulmonary
artery itself may be contracted in varying degree,
even to complete obliteration, a blind extremity or
rudimentary cord only remaining. Or the semilunar
valves may be fused together, and may form a mem-
branous, cartilaginiform or cretaceous septum with a
circular or slit- like opening. Or the contraction may
be below the valves at the apex of the right ventricle
—the conus arteriosus dexter— the cause being the
shrinking of the muscular tissue, subsequent to inflam-
mation (myocarditis). In one or two cases vegetations
like those described in case of aortic disease have been
found about the valves. In the rare cases met with
as originating at or after adult life atheroma may be
a cause or an inflammation due to direct violence, to
which the right ventricle and pulmonary artery, by
their superficial position, wouldseem to be more liable *
Jov convenience in clinical diagnosis, I think it best
to group the cases according to age.

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In infancy the patient will probably be the subject
of cyanosis, presenting the characteristics which we
have already considered. You will hear the murmur
loudly at the base, though in the small area of chest
presented in infancy you may not be able precisely to
locate it in the pulmonary region. The blueness of
surface, however, the venous distension, and the ex-
treme improbability of aortic disease at this period of
life, will leave little doubt as to the diagnosis. You
may safely infer that a patent foramen ovale, or an
aperture in the interventricular septum, co-exists with
the pulmonary obstruction, for such is the case almost
invariably.

In later childhood you will have more chance of
localizing the murmur, unless it be exceptionally loud.
You must bear in mind, however, that aortic disease
may possibly have been developed by rheumatic endo-
carditis subsequently to birth; therefore the differential
diagnosis between aortic and pulmonary obstruction is
now necessary. If the bruit be pulmonary, you will
probably observe a condition of cyanosis, at least in-
termittingly, and venous turgescence increased by
exertion and by coughing. Moreover, you may be
able to ascertain that the right side of the heart is
hypertrophied and dilated. There may be venous
pulsation. The following case, which occurred
under my own observation, affords many points of
interest: —

A little girl (L. S.), aged eight and a half, was ad-
mitted under my care at the North-Eastern Hospital
for children, on January 12, 1873; she seemed weak,
and was excessively pale, but presented no blueness nor
obvious dyspnoea. On auscultating the heart-region
a very loud rough first sound murmur was heard at

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163

the base, quite as intense at the aortic as at the pul-
monary point. The child had been ailing" occasionally
ever since birth, but there was no obvious symptom
except weakness. She was one of seven children, of
those, four were living-, one had been stillborn, and
one died during dentition. The mother was healthy,
and could give no account of " maternal impression."
I could not help giving a very doubtful diagnosis — it
appeared to me that it was quite as probable, from
the physical and general signs, that the obstruction
was seated at the aortic orifice as at the pul-
monary. As the case progressed, the next observed
phenomenon was diarrhoea, which began on January
13, and became very persistent and uncontrollable.
On February 1, hfemorrhoids were noticed. Progres-
sive enfeeblement occurred, the radial pulse became
scarcely perceptible, the hands very cold, while the
feet were fairly warm. A week afterwards delirium
was manifested ; the diarrhoea persisted, and there
was much abdominal pain ; emaciation continued, the
pallor increased, but throughout there was no cya-
nosis. The child died on March 10. At the autopsy
we found the lowest lobe of the right lung thickly
studded with masses of soft tubercle, varying in size
from a small pea to a large bean. The left lung also
was tuberculous at the apex. The large intestine was
ulcerated throughout its whole length, and the mesen-
teric glands were a complete mass of hard tubercle.
We found about an ounce of pale yellow serous fluid
in the cavity of the pericardium, and the heart itself
very small, pale, and contracted. The aorta and its
valves were quite normal, but the pulmonary artery
was very small in calibre (diameter four-tenths of an
inch), its walls firm and inflexible, so that it resembled

m 2

164

AUSCULTATION.

the aorta or a systemic artery. It was a pulmonary
artery in miniature, with valves minute but perfect.
The area of'a section across the aorta compared with that
of a section across the pulmonary artery was in the pro-
portion of three to one. The wall of the right ventricle
was greatly hypertrophied, so that it was thicker at
its thickest part than any portion of the left ventricle.
The foramen ovale was patent, the aperture being-
circular, with rounded edges, the communication
between the auricles quite unimpeded. There was no
imperfection of the septum between the ventricles ;
the valves were all healthy.

This case shows that we may have a loud murmur
of obstruction at the pulmonary orifice without
cyanosis. The signs strongly suggested aortic con-
striction, but there was one chain of circumstances
that led up to the diagnosis of pulmonary lesion — the
occurrence of general tuberculosis. The persistent
uncontrolled diarrhoea and wasting seemed to indicate
tubercular ulceration ; the post-mortem examination
showed tubercle abundantly scattered throughout
the body. Now tubercular changes in valvular
diseases of the heart, are, for a reason which I
will not stay to discuss for it is yet very obscure,
very rare. The great exception to this immunity
is in pulmonary obstructive disease. That con-
genital pulmonary construction predisposes to tubercle
has been noticed, especially by Lebert and Pea-
cock ; the observation is valuable as an element of
diagnosis.*

* I have discussed the subject of Pulmonic Murmurs in
Children more at length in " Clinical Lectures on Diseases
of the Heart in Children."— Vide "Medical Times and Gazette,
September 6, 1879, p. 255.

AUSCULTATION.

165

When adult life is attained, patients who present
signs of obstruction at the pulmonary orifice rarely
come under our notice. Besides the signs I have
already given you, enlargement of the right chambers
of the heart may now be more decided, or more readily
detected; in addition, a pronounced superficial systolic
thrill may be felt over the pulmonary area. There
may be considerable difficulty in determining whether
the pulmonary stenosis be congenital or acquired.
Though the congenital malformation is so fatal that
only about fifteen per cent, of the subjects reach the
age of twenty, some cases attain to a considerable
age. Instances are recorded, where the defect was
undoubtedly congenital, in which the subjects lived to
the age of forty (Kussmaul), fifty-seven (Peacock),
and sixty-five (Stolker), respectively. In nearly all
cases, however, inquiry will elicit the fact that there
has been some respiratory trouble, or some tendency
to lividity from infancy or early childhood. On the
other hand, in acquired obstruction there may be
a history of comparatively recent development of
symptoms ; a blow may have been received upon the
praacordial region which has set up myocarditis, or in
a patient past the prime of life you may observe such
evidence of degeneration of the systemic arteries
as would suggest the probability of atheromatous
change in the pulmonary artery.

Murmur with the second, sound in the pulmonary area,
due to incompetency of the pulmonic valves, may be
dismissed in very few words. It is very improbable
that you will meet with an instance. I only know of
one, recorded by Hope ; in this, the pulmonary artery
was dilated, and the apposition of the segments of the
valve thus prevented.

166

AUSCULTATION.

Double murmur — that is, murmur both with first and
second sounds — has been recorded in a few instances,
but is very rare. Of course it indicates obstruction,
combined with incompetence.

Having- finished the exploration of the pulmonary
valves, we now complete the investigation of the
right side of the heart by auscultating the tricuspid
area.

You may hear a soft blowing murmur with the
first sound limited to the triangular surface occupied
by the right ventricle, but most evident at the base of
the ensiform cartilage. If you have made this observa-
tion with care, and have excluded the probabilities of
extra-cardiac causation, you will conclude that the
murmur is due to regurgitation through a defective
tricuspid valve.

Remember that the conditions in regard to the
production of murmur are now exactly the reverse of
those which we have hitherto considered. A murmur
with the first sound, the site of which is the aorta or
pulmonary artery, indicates obstruction in one of these
vessels, the systole urging the blood through the
obstructed orifice. A murmur with the first sound at
either of the auriculo-ventricular apertures indicates
regurgitation through such aperture ; the contraction
of the ventricle whilst impelling, in the usual way, a
portion of the content of blood into the vessel of exit,
at the same time forces backwards, on account of the
gap left by the imperfectly apposed valve, another
portion into the auricle.

As regards the right side of the heart, the patho-
logical causes which bring about this result are dilata-
tion of the right ventricle and morbid changes in the
valves themselves. Of these the more common is the

AUSCULTATION. 167

former. When from any cause there is considerable
and continued venous congestion, the right ventricle
becomes distended and dilated. Emphysema of the
lung may dispose to this condition, but the most
common cause of all is disease of the left side of the
heart. Dilatation of the right ventricle follows disease
of the mitral valve when there is deficient propulsive
power in the left ventricle as consequence from cause.
The last result of such dilatation of the right ventricle,
is, that the curtains of the tricuspid valve, which under
normal conditions were competent to close the auricu-
lo-ventricular aperture during systole, are by the
circumferential traction of the walls of the widened
ventricle, withdrawn from the centre, so that their
edges do not perfectly meet. In systole, therefore,
blood regurgitates into the right auricle. The same
condition may result from a contracted state of the
papillary muscles to which are attached the ten-
dinous cords of any of the curtains of the valve.

The valve may have been altered by rheumatic en-
docarditis, though this disease very rarely attacks the
right side. It is very improbable that you will meet
with a case of tricuspid murmur with a history of
rheumatic origin without there being concurrent signs
of disease of the mitral or aortic valves. There may,
however, be a congenital affection of the tricuspid
due to endocarditis in foetal life, when disease of the
left chambers is almost unknown. Rupture of the
valve has also been recorded.

You must particularly note the concurrent signs of
tricuspid regurgitation. These are, first, the evidences
of hypertrophy and dilatation of the right side which
we have already discussed — the pulsation of the right
auricle may be obvious in the second right intercostal

168 AUSCULTATION.

space; secondly, tumescence of the veins of the
surface and often cyanosis ; thirdly, in some cases,
venous pulsation evidenced in the jugulars or in the
liver. The symptoms of tricuspid regurgitation are
dyspnoea, dropsy, and the distresses of heart-disease
in their gravest forms. For a very good account of
the secondary consequences of tricuspid insufficiency
consult Dr. Milner Fothergill, on » The Heart and
its Diseases."* It is very important for you to call
to your aid these concurrent signs, for whilst they
will assist you when you hear a murmur soft and ill-
defined as it often is, they will lead you to a diagnosis
when there is no murmur at all. Tricuspid regurgita-
tion without murmur is far from uncommon; thus
differing from mitral regurgitation, the reason being
the comparative feebleness of the right ventricle.

If you have arrived at the diagnosis of tricuspid
regurgitation, the prognosis is very unfavourable.
There is in this condition no chance of compensating
change to overcome the difficulty, such as exists in
most other morbid conditions of heart. Enhanced
power of the right ventricle but serves the more to
engorge the venous system by the greater regurgita-
tion ; greater strength of left ventricle, if attained,
would but increase by vis a tergo the tension in the
venous system, but it is not attained because the arte-
rial supply to the ventricle is diminished by the
existing conditions.!

You may possibly hear in the tricuspid area a
murmur which does not occur with the first sound,
but immediately before it. It is a presystolic murmur,
and indicates obstruction of the tricuspid orifice.

* London : Lewis, 3rd edition, p. 85.
+ Cf. Von Dusch, loc. cit. p. 230.

AUSCULTATION.

169

This lesion, however, in the absence of disease of
the other valves of the heart is almost unknown,
and its consideration may be conveniently deferred
until after the exploration of the mitral area.

Before proceeding- to auscultate the mitral area, I
shall ask you to consider certain sounds which are
heard in the interval between base and apex, and
even over the apex itself— sounds which are not due
to any organic disease of the valves.

I can show you many examples in which the first
sound of the heart, heard on auscultating between
base and apex— that is, over the right ventricle — is
rough in its character. The sound is not pronounced
enough to be designated a murmur, but the quality
of the contraction is not pure like that of the healthy
ventricle. I have found this to be distinctly the
case in some instances of dilatation of the right
ventricle, such as one meets with in chronic pulmonary
complaints. It occurs also in some cases of anaemia,
and is, in my opinion, evidence of a weak right
ventricle.

The sound may, however, be more than a mere
roughness : it may be termed a soft first-sound
murmur. This also may be due to anaemia, especially
when the condition of corpuscle-deficiency is associ-
ated with dilated right ventricle. That anaemic mur-
murs are occasionally generated over the right ven-
tricle, I have no doubt whatever. In these cases the
soft murmur may be heard only as far as the base,
or, and this much more commonly, it may disappear
at the aortic cartilage, and reappear with reinforce-
ment over the great arteries of the neck, in the
manner I have already described ; it is lost, how-
ever, at the apex of the heart. You may find such

170

AUSCULTATION.

murmurs in cases of any profound alteration of the
blood in advanced stages of tuberculosis and in
carcinoma.

But, going one step farther in degree, we may find
a blowing murmur heard as far as the apex, and even
localized at the apex — a murmur which, from its
quality and characters, is absolutely indistinguishable
from that of valvular disease. The great point, how-
ever, which differentiates it from the organic murmur
is its temporary or evanescent character ; its occur-
rence corresponds with a definite period in the history
of a disease, it fades away and ceases entirely when
the disease enters upon a new phase.

Murmurs having these characters have been de-
scribed as occurring (1) in chorea, (2) in the early
stages of certain acute febrile affections.

We will consider the explanations which have been
given of their occurrence — first in chorea. Every one
will agree that in a certain proportion of patients
suffering from chorea there is manifest a cardiac
murmur, sometimes at the base, but more commonly
at the apex. I have already said that this murmur
is in many cases very soft, often difficult to find, and
I think it is a fair inference that it is often overlooked.
I know I have often overlooked it myself in the early
examinations of a patient. Yet, when once it is
manifested, it may be observed to be persistent in
some cases, whilst in others it may completely disap-
pear, and leave no trace of heart-affection. What
is the pathology of this condition ? To begin with a
matter concerning which there is no doubt — in a con-
siderable proportion of the cases of chorea which
have proved fatal, vegetations have been found in
greater or less degree fringing the cardiac valves.

AUSCULTATION.

171

Organic disease of the valves will undoubtedly,
therefore, explain a certain proportion of the cases.
Happily, however, chorea is rarely a fatal disease.
Will the existence of structural changes in the valves
explain the murmur which, unlike that in other
valvular affections, entirely disappears ? Many ob-
servers say no. How, then, do they explain the
occurrence of the murmur which is heard over the
mitral area ? By assuming that there is in these
cases a peculiar contraction of the papillary muscles
of the ventricle, to which are attached the cords
which control the curtains of the valve, or else a
peculiar condition of the muscular walls of the ven-
tricle, whereby the apposition of the valvular curtains
is prevented, and consequently regurgitation takes
place into the auricle. You will understand that this
is mere hypothesis, and it seems to me very difficult
to accept it. That in chorea the muscle of the heart
should in some degree partake of the muscular per-
turbation which characterizes the disease is not im-
possible to realize, but whilst this would explain
irregularities in the time and quality of contraction
which undoubtedly do occur, it appears to me in-
capable of explaining the murmur. If the cardiac
muscle behaved in any spasmodic manner, surely the
murmur would present strange variations of site and
character ; sometimes it would be present and some-
times absent, sometimes soft, sometimes loud j where-
as it often presents no considerable variations from
hour to hour, # day to day, or week to week. Spasm
of the papillary muscles I cannot help but reject ;
disease of their muscular elements is out of the
question ; and any constant or consentaneous action
on their part, whereby they keep open the orifice

172

AUSCULTATION.

they are intended to close, seems also to impose a too
great demand upon our credulity. Parietal debility
of the ventricle seems to me equally difficult to accept :
it is quite unproved in these cases.

If we exclude the probability of a muscular causa-
tion, how shall we explain the non-persistent murmur
of chorea ? My answer is, that I see no difficulty in
concluding- that such murmurs are always due to some
change in or on the valves. The objections taken to
this view may be thus stated: — The endocarditis
which produces these changes of the valves is a
rheumatic endocarditis ; only a small proportion of
the sufferers from chorea are demonstrably rheumatic ;
therefore a changed condition of the heart-valves is
unlikely. The second objection is the formidable one
that endocardial changes of the valves do not pass
away, and the murmur which they occasion is per-
manent. As regards the first of these objections,
however, I have already shown how insidious may
be the advent and course of the endocarditis, even in
the form known as rheumatic, and that especially in
children, the articular symptoms may be trivial or
entirely absent. Moreover, there is no reason to be-
lieve that the form of endocarditis occurring in chorea
is of necessity rheumatic. It is the endocarditis
characterized by the presence of vegetations on the
endothelial surface which is met with in chorea ;
this is prone to occur on valves already altered by
rheumatic disease, but it can occur in the absence of
rheumatism. It is a mere hypei'plasia of the endo-
thelium which may exist in very slight degree, but
when it does occur the fibrine of the blood tends to
adhere to the thickened spot. The obstruction caused
by such a vegetation may readily occasion the mur

AUSCULTATION.

173

mur ; but under the repeated washing's of the current
of blood, the pedicle itself and the attached fibrine
may be washed away suddenly or gradually, and the
valve subsequently may present no trace of lesion.
I think that there is a very high probability that
fragments thus derived may block some of the
arterioles supplying- the corpora striata or other por-
tions of the cerebro-spinal motor tract, and that thus
is produced that form of chorea which is associated
with cardiac change. You must not misunderstand
me, however, and conclude that in my opinion this is
the exclusive pathogeny of chorea. It is to me highly
probable that just as epilepsy is induced in some in-
stances by actual disease of the brain and in others
by reflex irritations, so chorea may be the result, in
some cases of direct physical interference with the
arterial supply of the motor tract, in others of the
peripheral irritations (such as intestinal worms), and
probably in others of psychical stimuli such as fright
or emotional shock.

I shall teach you, therefore, that when in a case of
chorea you hear a murmur distinctly located at apex
or base you are to conclude that there is an organic
lesion of the mitral or aortic valves.

We turn now to the consideration of the temporary
systolic murmur which mav be heard over the apex
during- the course of certain acute febrile affections.

A murmur with the first sound, heard over the
apex of the heart but disappearing entirely with con-
valescence, has been observed in the course of small-
pox, erysipelas, and typhoid fever. The phenomenon
has been best investigated in the case of the last-
mentioned disease. In certain of the cases of typhoid,
about the end of the second week from the onset, a

174

AUSCULTATION.

first-sound murmur may be heard over the right ven-
tricle or just confined to the situation of the apex.
When localized at the apex the sound may have pre-
cisely the characters of an endocardial murmur, yet
as convalescence approaches it entirely disappears.
Certain other cardiac phenomena accompany it. The
impulse of the heart may be felt to be very feeble or
undulatory : the radial pulse may become inter-
mittent ; the second sound of heart may be heard to
be reduplicate. The signs show great enfeeblement
of the heart; this is so obvious that it does not need
discussion, and it is well known that some of the
subjects die suddenly in syncope.

We come to the inquiry — to what is the first-sound
murmur which is heard at the apex in these cases
due ? We may at once exclude any organic disease
of the valves, for it is known to be extremely rare
and almost unexampled for endocarditis to develop in
the course of typhoid, and the cases which have died
in syncope have shown no trace of structural altera-
tion of the valves. There is evidence, however, of a
decided change in the muscular structure of the heart.
M. Hayem, who has deeply studied this question, has
found evidence of myocarditis — an inflammation of
the muscular fibrillte — with granular and fatty de-
generation and a special form known as "vitreous"
change. Undoubtedly, therefore, there is structural
enfeeblement of the muscular walls of the heart.
We have again to encounter the question : How
can such enfeeblement induce the murmur ? And
first, is there a veritable regurgitation in such cases ?
M. Hayem considers that there is — the weakened
muscle can but imperfectly fulfil its functions, the
auriculo-ventricular orifice, powerless to resist the

AUSCULTATION.

175

force of the blood-current, allows itself to be passively
distended, or else the enfeebled papillary muscles can
no longer sufficiently restrain the valvular curtains.
Hence a practical, thoug'h a functional, insufficiency
of the valves.

The difficulty in accepting this explanation is far
less than that which besets the " dynamic" hypothesis
in the case of chorea. It seemed to me impossible to
admit that a neurosis, the special phenomenon of
which is spasm, should give rise to a long-lasting and
little-varying condition of patency of the auriculo-
• ventricular aperture ; I even found it difficult to allow
that mere passive weakness of the ventricle without
dilatation could permit of regurgitation. In the case
of typhoid, however, we have to deal not only with
general weakness but also with localized lesions. M.
Hayem says that in histo-pathological examinations
he has found patches of disease in the muscular
fibrillte disseminated here and there in a most irre-
gular manner* It is not difficult to assume, there-
fore, that there is a paralysis of certain of the papil-
lary muscles, and of necessity a condition of incom-
petence of the valves permitting regurgitation.

Let us consider the lessons derived from a case
under my own care. A young lady, aged nineteen,
whom I saw on the 10th day of well-marked typhoid,
manifested no cardiac murmur whatever. On the
11th day there was a very soft murmur with the first
sound, localized at the third left costal cartilage. On
the 13th day the bruit reached almost as far as the
apex of the heart ; it had all the characters of a blow-
ing endocardial murmur; in fact, had I heard it under

* See "Le Progres Medical," 24 Juillet, 1875, p. 416.

176

AUSCULTATION.

other circumstances, I am sure I should not have hesi-
tated to ascribe it to valvular disease, for it was heard
well within the mitral area, though careful ausculta-
tion showed that its maximum was a little right of
the apex. On the 15th day it was still heard as far
as the apex, but its maximum was at the third left
costal cartilage. On the 17th day of the fever, the
bruit was only heard in the last-mentioned situation,
but there was a distinct reduplication of both the first
and the second sounds of the heart. On the 01st dav
there was reduplication of the first sound only, the
bruit still audible as before. Convalescence went on
most satisfactorily, in a few days all trace of redupli-
cation had ceased, the basic murmur passed away, aud
slight antemic murmurs were manifest over the arteries
of the neck. On the 38th day the patient called at
my house in perfect convalescence, and presenting no
signs of cardiac trouble.

, This case was one of typhoid of not more than the
average severity ; the intestinal symptoms were well
marked, and the diarrhoea continued during the second
week in considerable degree ; the pulmonary signs
were a slight general bronchitis with condensation
about the base of the left lung which soon passed
through resolution ; the temperature taken in the
axilla never exceeded 104-2° F., nor the pulse 128,
and defervescence, commencing on the nineteenth day,
proceeded with almost perfect regularity. The cardiac
troubles seemed to be the most grave of those which
surrounded the case, and yet the course of the disease
appeared in nowise to be injuriously complicated by
them.

Let us review the circumstances of this case with
the view of explaining the murmur. In the first

AUSCULTATION.

177

place we have positive signs of enfeeblement of the
heart-muscle. A like weakness existed in marked
des- ree in the voluntary muscles; the " subsultus"
characteristic of typhoid was a prominent symptom.
It is found that in these cases the changes which occur
in the muscles of the heart occur also in the muscles
of the body. M. Hay em concludes from his able
researches that the cardiac fibrillae are diseased in like
manner and in like degree with the fibrillar of the
voluntary muscles. The existence of reduplication of
loth of the heart sounds was a very pronounced sign
of cardiac implication. Let us consider the concurrent
conditions. No one could doubt that in a case of this
sort there was a profound deterioration of the quality
of the blood due to the septic influences at work and
to the ''ensemble'' of adynamic conditions. But,
furthermore, there must have been a notable diminu-
tion of the normal quantity of the blood on which the
heart could contract, for a part of its volume had
drained away (and was still draining) from the
alimentary canal, and another part remained stagnant
in the congested lung. Such conditions were just
tantamount to a notable abstraction of blood.

Cardiac debility and deterioration of blood in quality
and quantity, therefore, are positive indications in our
case. Moreover, we have signs similar to those ob-
served in anaemia. The murmur first noticed could
have been taken for an anaemic murmur localized at
the commencement of the pulmonary artery. Soon it
became heard over the right ventricle; in convales-
cence it was gradually lost, and anaemic murmurs
were heard over the arteries. M. Hayem, speaking
trom other experiences, says of the murmur, "After
having been localized just at the apex near the nipple

178 AUSCULTATION.

it deviates to the right near the sternum, and tends
little by little to ascend towards the base. At the
same time the bruit becomes softer, and takes in a
more and more decided manner the character of an
anemic murmur."* We have here just the factors
which induce the anaemic murmurs which are heard
over the aorta and the great arteries.

I have long hesitated to adopt the theory of so-called
dynamic mitral murmurs, which I prefer to term adynamic
valvular murmurs. As I have just said, I feel bound to reject
the hypothesis in regard to the murmurs of the subjects of
chorea. In the case of the mitral systolic bruit, heard in
the acute fevers and in profound anaemia — a bruit which so
closely resembles that which is undoubtedly due to disease of
the valve, but which is nevertheless non-persistent— I am
now convinced, from personal experience, that there is tem-
porary mitral regurgitation. Dr. Hayden has published cases
illustrating such murmurs in the subjects of anaemia and
purpura, and of induced nervous prostration caused in one
instance by habits of masturbation, and in another by exces-
sive tobacco-smoking. In the case of the acute fevers it is
not difficult to accept with M. Hayem, the view that the papil-
lary muscles share in the disease which involves in various
portions the muscular structure of the heart, that thus their
co-ordinate action upon the curtains of the valve is impaired,
and leakage takes place through the imperfectly closed orifice.
In the cases of anaemia, &c. , it is probable also that the papillary
muscles are enfeebled. Guttmann says, " Inorganic mur-
murs at the mitral orifice are caused by the unequal tension of
the segments of the valve," which " is chiefly the result of
slight fatty metamorphosis of the muscular structure of the
heart, more especially of the papillary muscles, which takes
place whenever anaemia becomes profound" (cf. "Hand-
book of Physical Diagnosis," p. 287). Perl has stated that in
animals fatty degeneration of the heart may be experimentally
produced by repeated and copious venesection. Usually in

* " Le Progres Medical," 24 Jjiillet, 1875, p. 415.

AUSCULTATION.

179

cases presenting the adynamic murmur in the mitral
area the symptoms of grave mitral regurgitation are absent
— it is probable that the amount of blood gushing back
into the auricle and occasioning the murmur is small. When
the papillary muscles sufficiently recover their strength the
mitral cm-tains become properly apposed, and the murmur dis-
appears. Dr. Cuming, of Belfast, has described a case in
wbich there was a mitral murmur wiui the usual signs of
advanced organic disease — pulmonary engorgement, hasmo-
ptysis, anasarca, &c— and yet dissection demonstrated the
absence of anomaly or disease in the cavities, walls, or valves
of the heart. Dr. Hayden adds that he has also met with
two such cases. In Part II. I have quoted a case of profound
anasrnia in which there were the usual signs of advanced
organic valvular disease, and yet recovery and total di&apx'&ar-
ance of the murmur. In this case, relying on the evidence of
the sphygmograph, I made the diagnosis that the murmur was
adynamic (see Part II.). In the apex-murmurs, therefore,
occurring in typhoid and other acute fevers as well as in pro-
nounced ansmia and conditions of nervous shock, I think,
with Hayem, Hayden, Guttmann, Cuming, Bamberger, Hare,
and others, that there is veritable regurgitation due to en-
f eeblement of the muscle, chiefly of the papillary muscles, of the
heart.

You will remember, therefore, whenever you hear
a first-sound murmur localized at or near the apex in
a case of pronounced anaemia, to consider the pro-
bability of its occurring- independently of actual
disease of the mitral valve ; and, in tbe absence of a
history of rheumatic causation, to give a hopeful
prognosis, if only the condition of general anaemia
can be satisfactorily recovered from. And especially
if you hear such a murmur in a patient manifesting
typhoid fever (if there be evidence that no mitral
lesion has taken place previously to the occurrence
of the fever) you may predict with the highest pro-
bability that the sound will disappear, and that the
valves will not be affected.

n 2

180

AUSCULTATION.

Fugitive murmurs excluded, we now suppose that
a murmur is heard in the mitral area. You have deter-
mined the situation of the apex-beat, and you observe
that there is a bruit localized within, or having- a
maximum intensity within, the circumference of a circle
extending an inch around the apex. The phenomenon
indicates a morbid condition of the mitral orifice.

A murmur indicative of mitral lesion is met with as
probably the most common of all the signs of heart-
disease. Of the hundred cases of the various clinical
forms of disease which I have cited, fifty-eight mani-
fested the murmur indicating morbid change at the
mitral orifice.

By far the most common cause of mitral lesions is
rheumatic endocarditis. Of the fifty-eight cases just
mentioned thirty-two had suffered from rheumatism,
and of these twenty-three had been the subjects of
rheumatic fever; two, in addition, had suffered from
rheumatoid symptoms which occurred subsequently to
scarlatina. In seventy cases of mitral lesions noted by
Dr. Flint, rheumatism had occurred in fifty-five.
You will remember that I called your attention to the
frequency of pericarditis in acute rheumatism; a like
frequency exists as regards endocarditis— in fact, the
latter probably occurs rather more frequently than
the former. Whilst Hasse, Bamberger, and Lebert
give twenty-two, twenty, and seventeen per cent, re-
spectively as the proportion of cases of endocarditis
occurring in the course of rheumatic fever, Fuller and
others have fixed the percentage much higher. Not
at all infrequently the two diseases, endocarditis and
pericarditis, occur together during acute rheumatism.
I have already hinted that endocarditis, like pericar-
ditis, can arise and run its course in subacute rheu-

AUSCULTATION.

181

matism, where the articular symptoms are very slight
indeed — in fact, that in some cases objective symptoms
may be entirely absent. We must conclude, there-
fore, that endocarditis of the rheumatic form may
occasionally occur very insidiously, so that its origin
and course may be entirely overlooked.

Rheumatic endocarditis commonly starts from the
mitral valve ; in many cases the disease does not
extend further. It is an obvious corollary that the
mitral is the most frequent site of valvular deterio-
ration. Combining the figures of Willigk, Flint, and
Cockle, it would appear that the mitral is affected in
one hundred and sixty-six cases to one hundred and
thirty in which the aortic valves are diseased. The dis-
ease spreads from the mitral valve to the endocardium
lining auricle and ventricle ; its effects may often be ■
traced by the appearance of a milky patch of thick-
ened endocardium, stretching in a direct path across
the ventricle from the mitral to the aortic valves. The
pathological changes occurring in rheumatic endocar-
ditis consist, first, in a swelling and thickening of the
serous membrane and the substance of the valve, the
microscope showing an increase in the number of con-
nective tissue nuclei ; subsequently there is much de-
velopment of fibrous tissue ; lastly, there is a gradual
process of retraction of the newly-formed tissue just
as occurs in cicatrices. The morbid process may in-
volve the muscular structures immediately subjacent

there may be myocarditis, with the result of shorten-
ing of the papillary muscles and consequent retraction
of the cords and curtains of the valve.

Other causes besides rheumatic endocarditis may
produce lesion of the mitral valve and orifice. These
are identical with those which we have already con-

182

AUSCULTATION.

siderecl as affecting- the aortic valves — atheroma and
endocarditis of the villous (i.e., accompanied by vege-
tations) and the ulcerative forms. The valve may be
incrusted by calcareous salts, and rendered hard as
bone. Endocarditis may be induced by renal disease.
Lancereaux has recorded a very interesting* case, in
which, with a condition of contracted kidney, there
was disease of the mitral valve characterized by
thickening and the appearance of vegetations which,
under the microscope, were seen to be studded with
granules, distinctly proved to be deposits of urates.
The probabilities are very great that rheumatic endo-
carditis is due to the presence or excess in the blood
of the acid products of tissue disintegration, and that
the endocarditis met with in renal disease is due to
retention of the products which the kidneys are
unable to excrete. In the villous form of endocar-
ditis little excrescences may be seen fringing the
margin of the mitral orifice, especially on the auricular
side ; these have been often observed after death in
cases of chorea. The indications of ulcerative endo-
carditis we have briefly considered in connection with
the aortic valves ; remember that it may in like
manner attack the mitral ; recent observations have
shown that it may occur as one of the sequelae of par-
turition. Another cause of lesion of the mitral orifice
is rupture of the tendinous cords connecting the
curtains of the valve with the papillary muscles.
This is not very uncommon ; Flint found it in four out
of thirty-nine cases of mitral defect ; it may occur
from violent action of the heart. Again, the mitral
orifice may be rendered imperfect on account of
dilatation of the ventricle, whereby approximation of
the curtains of the valves is prevented. Lastly, but

AUSCULTATION.

183

very rarely, fusion together, or perforations, of the
mitral valve may be congenital.

When we come to review these various patholo-
gical causes in relation to their effect upon the
auriculo-ventricular orifice, we find that they can pro-
duce two well-marked varieties of lesion, as well as
a third variety, which is a compound of both the
others. Thus the orifice may be patent, the valve
imperfectly closing it- or it may be obstructed, the
outlet from the auricle being narrowed ; or it may be
both obstructed and pate?it, an impediment existing to
the outflow from the auricle, as well as an imperfec-
tion of the valve whereby it is prevented from closing
the orifice.

The first of these conditions is the most common.
By thickening and shrinking of the curtains of the
valve, by the presence of vegetations distorting them
or weighing them down, by their " pouching" with
aneurismal dilatations, by their perforation or ulcera-
tion, by swelling and shortening of the tendinous
cords attached to the curtains, by deformity or rup-
ture of the musculi papillares, by disease and retrac-
tion of the muscular wall of the ventricle, or by such
dilatation of it that the edges of the valves cannot
meet — by these and some other causes the mitral
orifice is prevented from closure at the time of the
systole of the heart. There is then said to be a con-
dition of mitral insufficiency; that is, the valve is
insufficient to close the auriculo-ventricular aperture.
The consequence is that at each contraction of the
ventricle a portion of the content of blood oUshes
backwards, through the space left by the imperfect
apposition of the valve, into the left auricle. There is
said to be mitral regurgitation. One consequence of

184

AUSCULTATION.

this condition is that the auricle is always ahnorraally
full ; the continuance of this leads to dilatation of the,
auricle, and the amount of sucli dilatation affords an
index of the amount of regurgitation. Furthermore,
the ventricle is of necessity incompletely emptied ;
from containing habitually too much blood it also
becomes dilated, and, in obedience to the law which
enables involuntary muscle to increase in bulk and
strength in order to overcome obstacles, it becomes
hypertrophied. This condition of hypertrophy with
dilatation has been called eccentric hypertrophy.
The consequences on the general system arising from
the leakage through the mitral orifice are, unless the
condition of hypertrophy exactly compensate for the
evils, insufficient supply of blood through the aorta,
whence diminished blood-pressure in the arteries,
sluggishness of flow in the capillaries from impaired
vis d tergo, and undue repletion of the venous radicles
and the general venous system. And when we come
to the right heart we find a condition of distension
(the pulmonary second sound is intensified, owing to
the heightened blood-pressure, as I have before
pointed out), and thus the right cavities may become
dilated. In the majority of cases the cause inducing
the condition of mitral regurgitation is rheumatic endo-
carditis. Mitral regurgitation occurred in forty-eight
out of my hundred cases of heart disease. Of these
twenty-six had suffered rheumatism, nineteen having
had rheumatic fever ; besides, two had suffered scar-
latina, wherein you know there are rheumatoid phe-
momena. Chorea existed in two cases, gout occurred
in one.

A quite different set of conditions obtains when the
mitral orifice is obstructed. The average circumference

AUSCULTATION.

185

of the normal orifice, according- to Bizot,is four inches;
its form is oval, the long- diameter being- one inch.
These dimensions are greatly modified by disease.
The cords, curtains, and muscles of the valve may be
stiffened into a rigid mass, or the edges of the orifice
may be obstructed by vegetations, in some cases very
small and insignificant, in others assuming the dimen-
sions of large polypi. In many cases the form of the
valve curtains and the shape of the outlet are singu-
larly altered. The curtains are, as it were, fused
together into an even tube, more or less conical, with
its smaller extremity downwards opening- into the
ventricle : sometimes this extremity is circular and
may be extremely small ; it may admit only the
thumb or the little finger, or be so minute as scarcely
to allow a small catheter or even a crow's quill to pass
through it. This variety is known as the " funnel-
mitral." Or the free extremity, instead of being- cir-
cular, maybe slit- like. Dr. Hilton Fagge has recorded
a case in which the slit was so narrow that it would
not admit a three-pennypiece edgewise. This is called
the " button-hole7' mitral. The septum formed by
the adherent valve-curtains may be incrusted with
calcareous salts so as to be of bony hardness. In
many cases, however, it is perfectly smooth and so
uniform in its conformation as a hollow cone, that it
seems to suggest that it must be a congenital anomaly ;
its perfect regularity appearing to contradict the
probability that it is the product of disease.

The effect of these conditions upon the auriculo-
ventricular aperture is the reverse of that produced
by the conditions which permit regurgitation. The
aperture guarded by the mitral valve, instead of being
widened, is narrowed— there is said to be mitral stenosis.

180

AUSCULTATION.

There exists an impediment to the flow from the
auricle into the ventricle — there is mitral obstruction.
Such an occurrence is not uncommon. Flint found
stenosis in sixteen cases out of thirty-nine instances
of mitral lesion. Of my forty-eight cases of mitral
disease, stenosis was declared by the physical signs to
exist in ten.

As I have before said, the regularity of form in the
case of the fused mitral valve has suggested the pro-
bability of a congenital causation. Dr. Hilton Fagge
inclines to this view in some cases, and thinks that a
rheumatic origin is comparatively rare. For my own
part, however, I am disposed to the view that nearly
all the cases are the result of rheumatic endocarditis
of a very chronic form. Of the ten cases I have
mentioned, four had suffered from rheumatic fever,
and two from subacute rheumatism ; in the remaining
four the causation was hypothetical. In undoubtedly
rheumatic cases, however, I have seen the funnel
mitral of the precisely regular conformation suggestive
of the congenital anomaly, and I think it must be ex-
plained by the involvement of the whole texture of
the valve by one or successive attacks of endocarditis
(which attacks, as I have before said, may occur with
little or no subjective sign), and by slow and regular
development of fibrous tissue with quasi-cicatricial
change. The great rarity of the positive evidence of
congenital anomaly of the mitral valve is in favour of
this view.

The secondary effects of mitral obstruction are quite
different from those of mitral regurgitation. The
most constant and most pronounced effect is upon the
left auricle, the wall of which becomes Tvypcrtrophied.

AUSCULTATION.

187

I have already cited a case under my own care illus-
trative of this point in considering the chronometry
of pulsations. It is quite clear that the hypertrophy
occurs in obedience to the usual rule — there is an
impediment to the outflow from the auricle to the
ventricle, and the muscle of the auricle becomes
hypertrophied to overcome the obstruction. Whilst
dilatation of the left auricle without hypertrophy is
characteristic of mitral regurgitation, dilatation with
hypertrophy is characteristic of mitral obstruction.
The left ventricle in mitral obstruction is found not
to be dilated. In some cases it has been observed
to be smaller than normal, its muscular wall has rarely
been found hypertrophied. When it has been thus
found tbe condition has been that formerly known as
concentric hypertrophy, which simply means hyper-
trophy without dilatation. In the great majority of
cases the left ventricle in mitral obstruction is found
not obviously abnormal, the condition thus differing
from that in mitral regurgitation wherein dilatation
and hypertrophy are the rule.

The consecutive changes in the right heart are alike
in regurgitation and obstruction, though the initial
causes are different. In both conditions there is im-
paired vis a tergo, and hence venous congestion and dila-
tation of the cavities of the right heart, but this is due
in the case of stenosis to the imperfection of supply
from the auricle to the ventricle with retention in the
auricle, whilst in regurgitation it is due to the retro-
grade diversion of the blood-stream through the mitral
aperture.

The subjoined diagrammatic sketches may aid you
to comprehend the conditions in mitral stenosis, as

188

AUSCULTATION.

distinguished from those in mitral regurgitation. They
are intended to represent vertical sections through the
left auricle and ventricle.

Mitral Stenosis
(Obstruction).
« Hypertrophied muscu-
lar wall of left auricle.

, Section of wall of left
veatricle.

c, Narrowed auriculo-
veutricular orifice.

(The arrow shows the direction of the current of blood at the
time of the production of the murmur.)

Mitral Insufficiency
(Regurgitation).

a, Dilated left auricle

b, Section of hypertrophied
and dilated left ventricle.

c, Patent auriculo-ventri-
cular orifice.

189

LECTURE VIII,
AUSCULTATION.

PART IV.

Differential diagnosis of mitral lesions — Rhythm — Chrono-
metry of murmurs — Vocal representation of murmurs —
Graphic representation of murmurs — Area of audibility —
Signs of mitral stenosis— Signs of mitral insufficiency-
Double mitral murmur — Combined murmurs — Diagnosis of
complex lesions.

Seeing that there are these well-marked varieties of
lesion of the mitral orifice, the question now occurs —
can they be detected and differentiated during- life ?
The answer is undoubtedly in the affirmative.

The previous examination of the patient has given
many data. We must exclude the evidence of any
departure from the normal as regards the right cham-
bers of the heart, for consecutive changes in these
can occur from either of the abnormal conditions of
the mitral orifice. Our examination of the left
chambers, however, may have afforded valuable evi-
dence. If we have found from the physical signs
that the left ventricle is dilated or dilated' and hyper-
trophied, the probability is great that if there be any
mitral lesion at all it will be one of regurgitation.
Palpation may strengthen this probability by evi-
dencing a systolic thrill • remember, however, to
time it carefully, for systolic thrill is rare and
presystolic thrill by far the more common. Suppos-

100

AUSCULTATION.

ing, on the 6ther hand, that we find little or no
evidence of displacement of the apex, hut a thrill
communicated to the finger distinctly antecedently to
the impulse of the heart — in this case the diagnosis of
mitral obstruction may he positively made. In some
such cases as I have before shown, the pulsation of
the hypertrophied left auricle may he visible in
vibration of the chest-wall, and its movement im-
mediately before the ventricular systole can be de-
monstrated.

It is but a small proportion only, however, of the
cases of obstruction of the mitral orifice that can be
thus diagnosed. The question now becomes narrower :
can the conditions be differentiated by auscultation
Twenty years ago it would have been declared
impossible. Contraction of the mitral orifice was
revealed by post-mortem examinations in a large
number of cases then as now. The diseased con-^
dition of the valve was not overlooked, but obstructive
and regurgitant lesions were no doubt mingled to-
gether in clinical diagnosis. A murmur was heard
in both classes of cases, but the rhythm of such
murmur was not recognized. Although some steps
had been taken in this direction by French observers,
Fauvel and others, it was not till Dr. W. T. Gairdner,
in 1861, by care fid clinical observation and philo-
sophical demonstration showed the characters, the
import and the causation of the murmur dependent
upon mitral constriction, that the diagnosis in any
considerable number of cases was affected. Further
observations, especially those of the late Dr. Hyde
Salter and Dr. Hilton Fagge, have contributed to
spread the knowlege of the methods of discriminating
the two conditions, but there is not the least doubt

AUSCULTATION.

191

that even now the condition of mitral stenosis in a
larg'e number of cases is not differentiated from the
regurgitant lesion. As to the ease with which this
diagnosis can be effected the opinions of good
observers vary; some say, with Dr. Hyde Salter,
that any one who should fail to recognize the mur-
mur of mitral obstruction " could hardly be con-
sidered a decently informed member of our pro-
fession;" others, with abundant opportunities of
observation, have failed to discover the murmur, and
have written papers to prove that it has no existence.
The truth lies probably between these two extremes.
The typical presystolic murmur any instructed clinical
observer who takes the necessary time and trouble
cannot fail to recognize, but there are some murmurs
so short, so slight, and so obscure that their re-
cognition and the determination of their rhythm are
matters of very great difficulty. Such obscurities are,
however, quite exceptional, and in the great majority
of cases it will be your own fault if you fail to
diagnose mitral stenosis when it exists.

We must first inquire : what is the rhythm of the
murmurs heard at the apex of the heart ? At the
base Ave know that the rhythm is very simple. Of
the murmurs there localized one is heard with the
first sound (systolic), the other commences with the
second sound (diastolic). At the apex we may have,
as at the base, a murmur coincident with the first
sound — systolic murmurs may occur both at the base
and apex— but, as a matter of fact, a murmur whose
origin is at the mitral orifice scarcely ever commences
at the same period of the heart's rhythm as the
diastolic murmur heard at the base. Such mitral
murmur occurs not with the second sound, but after

192

AUSCULTATION.

it. Cureful observation will show that a mitral
murmur is not diastolic in the sense of being- abso-
lutely coincident with the diastolic or second sound
of the heart, but that it occurs after the second sound
and before the first sound. It is now well known as
the presystolic murmur. A strictly diastolic murmur
of mitral origin — that is, a murmur commencing- at
the time of the second sound with a pause before the
first sound — although extremely rare, is not un-
known. Its mechanism will be considered hereafter.
It is unfortunate that the German authorities describe
all those murmurs generated at the mitral orifice
which are not systolic as diastolic. Under this term
they include the presystolic murmur — in fact, all
sounds that occur between the second sound and the
succeeding first sound. (Cf. Guttmann, " Handbook
of Physical Diagnosis," p. 289.) I have already
described to you the mechanism of presystolic thrill
and presystolic pulsation. The murmur which we
are now considering is produced by the same cause —
the forcing of the blood through the narrowed auric ulo-
ventricular orifice.

The term 'presystolic is not wholly devoid of objec-
tion. It is obvious that the systole of the heart
means the systole both of auricles and ventricles — the
presystolic murmur is presystolic only as regards the
ventricular systole, it is coincident with the auricular
systole. Nevertheless, the term has been so useful
that we cannot wholly discard it. Dr. Gairdner pro-
posed the term auricular -systolic, and this is for the
most part expressive of its physiological causation.
The propriety of the terms will, I consider, necessarily
vary as these are employed for the expression of the
clinical or the pathological conditions. For the latter

AUSCULTATION.

purpose, Dr. Gairdner's term is usually appropriate ;
but for clinical record it is better, in my opinion, to
use a term which shall fix the period of the murmur
in the heart's rhythm without even the semblance of
hypothesis. I do not think that the use of the words
" systolic" and " diastolic/' for the purpose of timing-
murmurs, is without reproach : but these, as well as
" presystolic," have become incorporate with our
notions, and we cannot well do without them. We
use them, however, on the principle expressed by the
phrase : If you know what I mean, what does it
matter what I say ? For precision, it would be much
better, in my humble opinion, if heart murmurs were
expressed in plain English and indicated by the
periods of the obvious and precise sounds of the.
normal heart. Thus, a systolic should be expressed
as a first-sound murmur, a diastolic as a second-sound
murmur, a presystolic as a h'forc-jirst-sound murmur.

From this preface let us turn to the practical
methods of discriminating- the rhythm of the mur-
murs heard over the mitral area and dependent upon
disease of the mitral valve. Here let me say, that
you must give full and long attention ; for the dia-
gnosis is easy if you take sufficient care, confused and
obscure otherwise.

First. — Endeavour to determine the exact position
of the murmur in the heart's rhythm. We may call
this the method of Ciironometry of Murmurs.
The principles of it I have already applied in the cases
of pulsations occurring over the cardiac area and the
phenomena of thrill. At the risk of frequent repeti-
tion I will again state the rule :— Apply your stetho-
scope over the point of maximum loudness of the
murmur, and place the tips of the fingers on any

104

AUSCULTATION.

point of the chest where you can feel the impulse of
the ventricles or over the site of the pulse of the
carotids. You auscultate at the same time that you
feel the pulsation of the heart or of one of the great
arteries near it. The cpiestion which you have to ask
yourself is this : Is the murmur which I hear coin-
cident with the first sound of the heart, or is it
previous to it and directly terminated by it? Do not
run away with the notion that without all this care
you can determine the question : you may not he able
even to distinguish the first sound from the second
sound. What said one of the greatest authorities,
the late Dr. Stokes ? — " So great is the difficulty, that
we cannot resist altering our opinions from day to day
as to which is the first and which is the second
sound."'"' There can, I think, be no doubt that the
great reasons why in times past the condition of
mitral stenosis remained undistinguished from that of
regurgitation, was that the murmur was judged to be
systolic, and the first sound was taken for the second
sound. In cases of stenosis, the mistake is peculiarly
easy, for the first sound is usually very short, sharp,
and sudden, much resembling the second sound.
These considerations are cpiite enough to inculcate
lessons of care in observation, and the absolute
necessity of timing the murmurs. If the murmur be
systolic you will hear it commence at the same instant
that the finger is sensible of the cardiac pulsation.
It is produced, as you know, by the reflux current
forced into the left auricle by the ventricular contrac-
tion. It is a truism, therefore, to say that its period
of production is the period of its cause — i.e., the

* "A Practical Treatise on Diseases of the Heart,'' 3rd
edition, 1862, quoted by Dr. Fagge, loc. cit.

AUSCULTATION.

195

ventricular systole. Commencing- immediately with
the full force of the contraction, it may last through-
out the whole systole, or it may become feebler and
inaudible as the ventricle becomes emptied. In other
words, it may be short or long- ; commencing with the
systole, its duration may be the whole or a part there-
of. Such is the first-sound murmur, — the murmur of
mitral re°-ur°-itation.

Suppose now that the murmur which you hear be
not coincident with the systole. A.t the moment that
your finger becomes sensible of the impulse of the
heart against the wall of the chest, the flap or thud
of the first sound is audible. Preceding this, how-
ever, and soon after the second sound, a rou°-h murmur
is heard. This murmur also may be either short or
long; it may commence immediately after the second
sound, or it may occur momentarily before the first
sound, but the latter always terminates it as with a
sudden full stop. The mechanism I have before ex-
plained— it is the sound produced by the effort of a
hypertrophied auricle in urging the blood through a
narrowed mitral orifice. This presystolic, before-
first-sound murmur, is absolutely diagnostic of mitral
stenosis.

Secondly. — In order to help you to realize the dis-
tinctive characters of these sounds, I would call your
attention to a method of Vocal Representation
of Murmurs. The " bruits" heard over the heart-
region have received since the time of Laennec many
names according to their narure and quality. Thus
we have bellows' sounds, filing, grating," rasping,
croaking, crowing, whining, caterwauling, and blub-
bering sounds, or musical or sibilant sounds. Bouil-
laud imitated the character and pitch of the sounds

o 2

i'j<;

AUSCULTATION.

by letters, the pronunciation of S expressing the ex-
treme of* sibilant murmurs of* high pitch, R represent-
ing- those of" low pitch. These illustrations are all of
some value, as enabling- one to note the variations in
character of any given murmur from time to time,
and thus indicating changes favourable or unfavour-
able, or the persistency of the lesion. Any of the
illustrations just given may be applied to the mur-
murs produced by the valvular conditions we have as
yet considered; the sounds, therefore, cannot be con-
sidered diagnostic. Valuable help, however, may he
derived from a consideration of the sound in the
differential diagnosis of murmurs heard over the-
mitral area. The murmur of regurgitation may have-
almost any of the characters just described, hut not
so the murmur of ohstructiou. This latter is almost
invariably rough; it has been called a "churning,"
" grinding," or " blubbering" murmur. In my own
opinion, in typical cases, it may he best illustrated as
" rolling," or " bubbling," resembling the sound of
air rising through water. You may easily realize its
distinctiveness from the systolic murmur by these
simple considerations — the systolic fades off" butnevei"
terminates abruptly, the presystolic always stops sud-
denly. I have frequently illustrated this by the sub-
joined vocal illustration, the sound of up" indicating
the abrupt termination of the pres}rstolic murmur.

Sound of Systolic Sound of Presystolic

Murmur. Murmur.

Hooh — hoof — ruff. Up — rvp — rr. rr. rvp.

Thirdly. — We come to a plan which we owe to-
Dr. Gairdner, and I know of none which is more
valuable to fix upon the mind the phenomena of the

AUSCULTATION. 197

murmur, and to serve as a method of record. Wo
may term this the method of Graphic Represen-
tation of Murmurs. To represent all the facts
and conditions, I have combined Dr. Gairdner's plan
with a chart which I have modified from Dr. Salter.

The upper portion of this diagram represents the
conditions of the auricle and ventricle during- three
■cardiac pulsations. Each such pulsation or cycle is
divided into six equal parts, which are denoted by the.
squares. The squares which are shaded denote that
the chamber (auricle or ventricle) contains blood,
whilst the black squares indicate that it is replete —
i.e., at its maximum of distension. The squares
marked C denote contraction or systole. The upper
.line of squares A pertain to the auricle, the lower V
to the ventricle. Taking the auricle first and pro-
ceeding from left to right, we see that it is receiving

Fig. 6.

i i

PAUSE

THE NORMAL CARDIAC RHYTHM.

blood during the period indicated by the first four
squares, and that at the fifth it has arrived at its
maximum distension. Then follows C, its systole or
■emptying through muscular contraction. Looking at
the ventricular line V, we see that the systole lasts
•during the first two squares, or two-sixths of the

c c

AUSCULTATION.

csyele, that during the following three it is in diastole
■or receiving blood, and at the sixth it has arrived at
its maximum distension. Then the cycle is in each
case repeated. Now, we are enabled by a glance at
the diagram to note the relative condition of auricle
and ventricle at any given moment of the heart's
action ; we have only to compare the upper sections
with the lower. Thus we see that whilst the ventricle
V is in systole, the auricle A is in diastole : that A,
having at last become distended, contracts, while V is
yet in diastole, and completes the repletion of V, which
recommences the cycle by contraction. Again, by a
horizontal line below, we have a means of comparing
these conditions with the sounds of the normal heart,
the vertical lines 1 and 2 denoling the first and the
■second sounds respectively. You will see that the
latter occurs very soon (about half a square) after the
ventricular contraction, the first sound lasting during-
two squares.

We have thus a very simple and concise method of
registering murmurs, their position in the cardiac

Fio. 7.

SYSTOLIC 0

Ft FIRST-SOUND

MURMUR.

DIASTOLIC

. OR SECOND-SO

UND MURMUR

rhythm and their duration. Taking the horizontal
line to express the duration of the cycle, and the ver-
tical lines to denote the first and second sounds, we
have merely to indicate by shading the place and

AUSCULTATIOX.

estimated length of tlie murmur. Thus, the simple
systolic and diastolic murmurs heard at the base of the
heart, would he indicated by the diagram (fig. ?)■
The one commences with the first, the other with the
second sound.

The rhythm of the first- sound murmur heard at
base and apex is precisely similar. The upper line of
this diagram would alike express the sounds of aortic
obstruction and mitral regurgitation. Of course a
note of the area of audibility and maximum intensity
would at once indicate the diagnosis.

We will now consider how this method illustrates
the differential diagnosis between the murmurs of
mitral reg-ursitation and mitral stenosis. The sub-
joined diagram you will readily understand from the

Fig. S.

to I

i. i
SYSTOLIC OR FIRST SOUND MURMUR.

i ^illllllll

' 2

PRESYSTOLIC OB BEFORE -FIRST SOUND MURMUR

explanation I have already given. It shows how the
systolic murmur starts with the first sound, and the
presystolic leads up to the first sound; whilst a glance

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AUSCULTATION.

fit ttte upper section of the diagram indicates the
cardiac conditions at the time of the production of
the murmurs. The first-sound murmur occurs with
V C C, the ventricular contraction ; the presystolic
with A C, the auricular contraction. It is possible
that, as the diagram shows, the presystolic murmur
may commence during the distension of the auricle,
and previously to its actual systole.

Having considered the rhythm of the murmur, we
have yet another aid towards the differentiation of
mitral stenosis from mitral regurgitation in the deter-
mination of the area of audibility.

It is rare for the murmur of stenosis to he heard
to any considerable degree below or outside the situa-
tion of the normal apex. As I have before said, the
conditions of hypertrophy and dilatation of the left
ventricle, which cause the apex- beat to be discernible
externally and inferiorly to the normal position,
seldom coexist with mitral stenosis. A murmur,
therefore, heard left of the cardiac area in conjunc-
tion with the signs of ventricular enlargement is
unlikely to be a murmur of mitral obstruction. Ex-
ceptions to this rule occur when hypertrophy of the
ventricle from other causes coexists with mitral
stenosis. 1 have recorded a case in point in which
there had been repeated attacks of pericarditis with
numerous adhesions.* Observers have agreed that
the murmur of obstruction is a localized murmur — it
is seldom audible far from the apex. Again it is
said to have its maximum intensit}' at the apex. To
this last conclusion, however, I shall have to demur :
it has been an almost invariable experience with me

Vide Medical Times and Gazette, June lOfch, 1874. p. 34.

AUSCULTATION.

201

that the presystolic murmur is loudest at a point in-
ternal to (i.e., right of) the apex-beat. It is usually
audible over a portion of the normal area of the right
ventricle, but seldom as far on the pulmonary car-
tilage, but is suddenly cut off at the left apex and is
inaudible, or scarcely audible, left of the apex.

Let us contrast this with the murmur of mitral re-
gurgitation. This systolic murmur may have a very
small area of audibility around the apex, but its
maximum is never just internal to this point. On the
contrary, in a large majority of cases it is louder a
short distance outside the apex than at the apex itself.
When it is of considerable intensity, the sound of the
murmur may be carried towards the axilla and may
be audible over the axillary part of the chest-wall :
it will probably disappear as the stethoscope is carried
to the back, but may again become evident between
the scapula?, especially in the interval between the
angle and the spine of the left scapula.

In exceptional cases both the systolic and the presystolic mur-
murs, generated at the mitral orifice, may be conducted towards
the right instead of to the left apex. In these there is an unusual
conduction of the murmur, due, accordingto my observation and
experience, to the fact that the disease of tbe valve has involved
that portion whose papillary muscles and cords are connected
with the inter- ventricular septum. So the vibrations are con-
ducted by the dense material through the septum to the sternum
and the right apex, ami the maximum of the murmur is in the
tricuspid area. In like manner a tactile thrill of systolic rhythm
may be abnormally conducted towards the right. I have also
found the presystolic murmur under like circumstances con-
ducted to the tricuspid region. Where the bruit is loud and
musical or whistling, I consider that we may infer that the
diseased portions of the valve have undergone calcareoits trans-
formation. Guided by this experience, I made, in a case which
presented a presystolic murmur having these characters (but
whicli ceased at the later stages of the disease), as well as a

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~ ~ AUSCULTATION-,

systolic mitral murmur, the following diagnosis :— That there
mitral constriction, the characteristic presystolic murmur
1 whlch Lad beeQ conducted by dense material to the inter-
ventricular septum and thence towards the right apex ; that
the valve-aperture was probably a calcareous ring; that the
murmur had ceased to be audible because the left auricle had
become dilated and its muscle enfeebled ; that there was, in
addition, incompetency both of mitral and tricuspid valves,
with hypertrophy and dilatation of each ventricle. At the
autopsy, inwhichlwas kindlyassistedby Dr.Hamiltonof Canon-
bury, who had had daily charge of the patient, the diagnosis
was exactly confirmed. The left auricle was very large and its
walls extremely thin. Seen from the auricular aspect, the
mitral orifice was of button-hole shape, with rigid borders, and
allowing abundant regurgitation ; the right boundary was con-
verted into a dense calcareous mass with numerous hard and
rough projections. The tricuspid orifice was moderately in-
competent, but its valves normal. It thus appears that in
certain cases of murmurs heard in the tricuspid area we may
be able not only to infer that the morbid change is at the mitral
orifice, but to diagnose the nature of the deposit. (Cf. "Pro-
ceedings of the Medical Society of Loudon," vol. iii., p. 145.
and Medical Examiner, Jan. 25, 1877, p. 65.) Guttmann, fol-
lowing Naunyn, says that in very exceptional cases a mitral
systolic murmur is of greatest intensity in the second left, inter-
costal space. Naunyn believes this to indicate hypertrophy of
the left auricular appendix: — "That, as in every case of
mitral insufficiency the systolic regurgitant current of blood,
rushing from the left ventricle, enters not only the corre-
sponding auricle, but penetrates also to its appendix (the cavities
of both parts being continuous), the further the latter passes
round the pulmonary artery, and the nearer its apex comes to
the anterior chest- wall, the more favourable are the conditions
presented for the propagation of the mitral murmur through
the left auricle into the appendix and theuce to the thoracic-
parictes (Guttmann, "Hand-book of Physical Diagnosis,"
Sydenham Society's translation, p. 2S9). This seems to me
a far-fetched theory : it is far more likely that the murmur, as
in the instances I have quoted, is abnormally conducted by
the diseased structures at the iusertion of the right curtain of
the mitral valve.

AUSCULTATION.

A little consideration will, I think, enable you to
realize the physiological causes of the differences in
sire of the two murmurs. A reference to the diagram
illustrating the conditions in mitral stenosis (p. 188)
will remind you that the direction of the current — i.e.,
the line of convection of the murmur — is from the
auricle to the apex of the heart. It would seem,
therefore, prima facie that the "bruit" should be most
audible at the apex. We must recollect, howevei-,
that at the time of production of the murmur the
apex is not close to the wall of the chest ; its position
is slightly internal to that which it occupies when the
ventricle strikes the chest-wall, and a space inter-
venes. These considerations to my mind explain the
position and the limitation of the murmur. In re-
rjurgitation, on the other hand (see fig. 5), the direc-
tion of convection is contrariwise ; you might say
that the sound ought to be carried to the region of
the left auricle. Why is it not so 1 Surely because
the walls of the left ventricle conduct the sound in a
direct line to the apex, and thence to the ear. At the
moment of production of the first sound the apex is
in direct contact with the chest-wall, and occupies a
position left of that which it occupied previously.
The muscular ventricle, the thoracic parietes and the
stethoscope, heing in close apposition, constitute one
solid conductor through which the sonorous vibrations
travel in uninterrupted course to the ear. Both these
murmurs maybe intensified by causing the patient to
use muscular exertion ; but especially the presystolic*
The latter is apt to vary in intensity and audibility : it
may be absolutely inaudible till the patient is put
through a little walking exercise.

We will now sum up our auscultatory evidence.

AUSCULTATION.

A rough murmur is heard antecedently to the Jirst sound,
■and abruptly terminated by it: its maximum intensity
being slightly internal to the normal apex. The condition
is one of Mitral Stenosis.

We will devote a short time to the clinical history
•of these cases, and the phenomena which you may
observe during- your observation of their progress.
The late Dr. Hyde Salter noticed the remarkable
proclivity of the subjects of mitral stenosis to lieemo-
ptysis. He recorded this as occurring- in six out of
eight cases. I have no doubt, however, that this was
an exceptional frequency; for out of sixteen cases
recorded by Dr. Fagge, J find haemoptysis noted only
in three, and in seventeen rases under my own care it
•occurred also in three. Though these figures modify
those of Dr. Salter, they support his conclusion that
haemoptysis is a frequent symptom in mitral obstruc-
tion. The cause is no doubt the backward pressure
exerted by the contraction of the auricle (opposed as
it is by the obstruction at the auriculo-ventricular
outlet) upon the pulmonary veins; hence there is
-congestion of tlie pulmonary capillaries to the point
of rupture. In mitral obstruction the capillaries
suffer the direct pressure of the contracting auricle,
whilst in regurgitation the auricle intervenes as a
■dilatable cavity between the contracting ventricle and
the pulmonary veins.

The next point of interest in the clinical history or
these cases is the proneness to embolism of one of the
cerebral arteries, or of some arteiw of the. lower limb.
Remember, therefore, to inquire carefully into the
-cerebral conditions of all patients whom you find to
manifest the signs of mitral stenosis, and conversely
in cases of sudden paralysis, apparently of cerebral

AUSCULTATION.

origin, be mindful to explore the mitral region. Yon
will readily understand bow the contraction of the
auricle may detach a pellet of fi brine or a pediculated
vegetation from the endocardial surface, or from the
margin of the auricula-ventricular orifice, and trans-
mit it into the direct current of blood urged by the
ventricle into the arteries.

With regard to other symptoms, the subjects of
stenosis are in most respects affected in like manner
with the subjects of insufficiency. As I have said
before, the secondary effects upon the right chambers
of the heart are alike in both cases. So we have in
both cough, dyspnoea, and the evidences of congestion,
pulmonary and general, and in the end, dropsy, &c.
In one point, in my experience, the cases are slightly
different — the subjects of stenosis are more liable to
variable symptoms and spasmodic troubles.

Mitral stenosis excluded, we turn to the other
condition.

A murmur is heard with the .first sound, or entirely
occupying the ■place of the first sound in the cardiac
rhythm : its maximum, at, or external to, the position of
the apex-heat . The condition is that of Mitral In-
sufficiency.

In these cases of mitral regurgitation, when the
lesion is not compensated by exactly sufficient hyper-
trophy of the ventricle, the symptoms may be any of
those which we have already considered early in these
lectures. It is unnecessary to revert to them.

With regard to Prognosis in stenosis and insufficiency
respectively, opinions are divided. For my own part,,
whilst agreeing that in stenosis there are certain special
dangers, I am inclined to the belief that on the whole
compensation is more certain and more persistent.

AUSCULTATION.

We come now to consider the case wherein the
conditions we have just discussed coexist.

A murmur is heard, antecedently to the first sound, and
in addition a murmur is heard supplanting, or occurring
with, the Jirst sound. The condition is one of combined
Mitral Obstruction and Mitral Regurgita-
tion.

In a very small minority of cases the sound is
distinctly double. At the situation of the apex-beat
you hear a murmur with the systole, then a pause,
then a murmur which seems to be diastolic, and then
a short pause before the recurrence of the first-sound
murmur. You can convince yourself, by carefully
timing, that the murmur which appears to be diastolic
is really subsequent to the click of the semilunar valves.
I am aware that in saying- that there may be a pause
between a presystolic and a systolic murmur, I am
diverging' from the teaching- 0f some who have deeply
studied the question, but I do not speak without prac-
tical experience. I had an opportunity of observing* a
case in which this was exemplified. At a spot just in-
ternal to the apex there were two distinct murmurs
separated by pauses. The explanation of the pheno-
menon appeared to be given to another case under my
care, in which the only endocardial murmur was pre-
systolic, but this was separated by a decided pause
from the first sound. It was of such character that
I called it a diastolic murmur. In this case the post-
mortem examination revealed extreme narrowing of
the mitral orifice, but in addition the ventricle was,
in great measure, filled by vegetations depending* from
the lower surface of the valve. The latter condition
seemed to me to explain the peculiarity of the murmur
— the ventricle being already partially filled by the

AUSCULTATION.

vegetations, the murmur occurred only at the early
part of the diastole, ceasing- early because the small
ventricular space lei't became quickly replete.

In the great majority of cases the double mitral
murmur can be readily resolved into two murmurs,
having' the distinctive characters which we have
already discussed. The systolic element of the com-
pound murmur is widely diffused, but the presystolic
is heard only over its usual limited area. In the
near neighbourhood of the apex the sound may be
distinctly double: you hear the rolling presystolic
murmur pass into the prolonged systolic. Or the
presystolic may abruptly cease with a sharp first
sound from which a soft systolic murmur tails off. In
many cases, however, there is no spot where you can
hear the two murmurs at one and the same time.
This was well described by the late Dr. Salter, who
cited a case. In Dr. Salter's words — ( 1 At the apex
a grinding bruit is heard, immediately Receding an
upparently natural Jirst sound, and terminated by it.
On working back well into the axilla, and not until
the axilla is quite reached, a systolic murmur begins
to reveal itself, increasing in distinctness as you work
round to the back, where it is loud and strong. It is
audible over the whole of the left side of the back.
On returning again to the front, to the region of the
apex, it is quite lost, and the presystolic bruit is again
heard."* I have no doubt that you will meet with
examples verifying this description.

The physical cause of mitral murmurs can be ex-
plained according to the same principles as those
which govern murmurs generated at the aortic orifice.

* Lancet, July 24tb, 1869, p. 114.

AUSCULTATION.

As regards the mitral systolic murmur we can thus
explain its production : — So long- as at the time of
systole the curtains of. the mitral valve are perfectly
apposed there results only the sound of valve-tension
— the normal first sound. Vibration is prevented by
the coaptation of the valve-curtains. If from any
cause, however, the segments do not meet, their
borders are free to vibrate in the stream of blood,
which of necessity regurgitates through the orifice
left by their imperfect approximation. Where the gap
is considerable, or the disorganization of the valve
extensive, the normal sound of valve tension is alto-
gether lost by the murmur entirely replacing it. When,
however, a considerable portion of the valve curtains
are capable of flapping back, the murmur is affixed to
the sound of their closure. Such murmur is some-
times termed post-systolic. It must not be forgotten,
however, that the sound of valve tension may be that
of the tricuspid ; if the murmur, when heard at the
axilla and back, is accompanied by the flap of the
valve, it may be fairly inferred that a considerable
portion of the mitral valve is competent. The vibra-
tions communicated to the boundaries of the imper-
fectly closed orifice are not conveyed by the current,
as in the case of the aortic regurgitant murmur, for
in such case the " bruit" would be heard over the left
auricle. They are, however, conducted by the solid
structures, usually to the wall of the ventricle and the
left apex, exceptionally, as lately explained, by good
conductors, to theright apex and the adjacent sternum.
The mechanism of the mitral systolic murmur is
simple, and its occurrence pathognomonic of mitral
reo'uro-itation. The loudness of the murmur is by no
means an index of the amount of regurgitation. In

AUSCULTATION.

209

the earlier stages of valvular insufficiency it may be
almost confidently stated that there can be no re-
gurgitation without murmur. When, however, as in
the last stages, the left ventricle becomes very feeble,
the. murmur may cease to be generated. So the en-
feeblement or cessation of a mitral systolic murmui ,
when there are signs of increasing cardiac distress, is
an evil omen pointing to failure of the left ventricle. On
the other hand, when the disappearance of a mitral
murmur is coexistent with amelioration in cardiac
symptoms, and especially with enhanced power of the
left ventricle, as evidenced by the cardiograph and
sphyg-mograph, theprognosis is good; the regurgitation
has been probably due to muscular enfeeblement, and
not to structural disease of the valve.

The presystolic mitral murmur I consider to be due
to vibrations communicated to the abnormal mitral
curtains, the solid structures in union with them, and
the wall of the left ventricle, by the current of blood
issuing under pressure through the narrowed mitral
orifice during the diastole of the ventricle. Such
may be induced by the blood pressure in the
auricle and pulmonary veins, independently of the
auricular systole • may be reinforced by contraction of
the auricle during the period of diastole, especially at
the conclusion of the period ; or may be initiated only
by the auricular systole just before the contraction of
the ventricle.

The mechanism of the presystolic murmur is more complex
than that of the systolic, because the factors are more
numerous and the conditions more variable. The sounds
heard in connection with mitral stenosis can, I consider, be
referred to the following types (see Fig. 9) :

I. Reduplications, or seeming reduplications, of the normal
sounds without murmur. I have already (p. 119) called atten-

L>10

AUSCULTATION.

tiou to this as presumptive evidence of mitral narrowiug. Au
apparent reduplication of the second sound is the most com-
mon. Of thirty-seven cases in ■which I have made the diag-
nosis of mitral obstruction, I have found such reduplication
in eleven cases. This agrees with the experience of Guttmann
(one in three cases) and Hayden (thirty in eighty-one). I
have already explained the mechanism of its production. I

Fig. 9.

Diagram illustrating varieties of sounds observed in mitral

stenosis.

A, reduplication of second sound. B, reduplication of first
sound. II. Prolonged murmur from second to first sound.
III. The same, with reinforcement during its progress. IV.
Presystolic murmur, with reinforcement at its close. V. Post-
diastolic murmur.

believe it to be due to the sudden fioating-up of the valve-
curtains of the mitral, owing to the increased pressure in the
left auricle and pulmonary veins ; thus the valve is put on the
stretch, and the sound of valve- tension results. Occurring at
the earlier part of diastole, this appears like a doubling of the
second sound. . Occasionally such may be the only auscuita-

AUSCULTATION.

211

tory sign of mitral stenosis, for the presystolic murmur may
be absent. We have abundant experience that this murmur
may appear and disappear ; at the periods of its absence the
seeming reduplication may alone be heard. Much more com-
monly, however, there is a short pause after the second
element of the reduplication, and then a murmur of the pre-
systolic character such as we shall presently discuss. In three
oases I have noted reduplication of the first sound in connec-
tion with mitral stenosis. I have discussed the mechanism
of this, and have explained it by the view that in these cases
the tension of the valve curtains takes place late in diastole —
that is, synchronously with the auricular systole. Occurring
just before the systole of the ventricle, this gives rise to a
seeming reduplication of the first sound.

The following types of sound, generated by the conditions of
mitral stenosis, are forms of the presystolic (before first sound)
murmur.

II. A murmur is heard occupying the whole of the interval
between the second sound and the first sound (Fig. 9, II.)
Usually this murmur receives a distinct emphasis near its
termination ; it often concludes with a rattle or roll, just as it
is terminated by the sudden flap of the ventricular systole.
You wdl observe that the murmur, so far as regards rhythm,
may be identical with that of aortic regurgitation. Inamajority
of cases the diagnosis between the two conditions will not be
difficult. The area of audibility of the murmur of aortic
reflux is usually notably different (as formerly pointed out) to
that of mitral narrowing. Nevertheless, it is possible that
difficulty may be experienced in the differentiation, for, as I
have said, occasionally, though very rarely, the area of audi-
bility of an aortic diastolic murmur is at the apex. In such
cases the diagnosis may be peculiarly difficult. My own
belief is that the physical signs in the two conditions may be
very similar— there may be in each, according to my own
observations, a thrill of presystolic rhythm, and in each a
seeming reinforcement of the murmur just before the ventri-
cular systole. Indeed, the physical conditions in the two
cases are very similar. In case of a presystolic mitral mur-
mur such as this, a stream of blood is pouring during the
whole period of diastole from the left auricle, and the veins in
communication with it, into the left ventricle; vibrations

P 2

ai2

AUSCULTATION.

capable of conveying sonorous impressions are communicated
to the ventricle during the whole period, and are intensified at
the close when the auricle adds the force of its contraction to
the expulsive powers. In case of the aortic diastolic mur-
mur vibrations arein an analogous manner communicated to tbe
leftventricle (in the instancewe are now particularly considering
to the apex of the left ventricle very probably, because the
reflux current impinges directly on the upper segment of the
mitral valve*) during the whole of diastole, owing to the
gushing of the refluent stream through the chink occasioned
by the imperfect closure of the aortic cusps, the backward
impetus being due to the tension in the aorta and the whole
arterial system, plus the gravity of the blood column. The
physical conditions, therefore, in the two cases are closely
analogous— a stream being urged under pressure during the
whole period of diastole through narrowed orifice into the
left ventricle, and the conduction of the vibrations being to
the apex of the ventricle. The difficulty is by do means a
merely imaginary one. Dr. Flint has recorded two cases
in which murmurs presenting typically presystolic characters
had been present, and yet post-mortem examination showed the
absence of mitral stenosis and the existence of aortic insuffi-
ciency. In regard to these cases, Dr. Flint says, in both " the
mitral direct murmur was loud, and had the character of
sound which I suppose to be due to vibration of the mitral
curtains" (American Journal of Medical Science, vol. xliv.)
Dr. Charlewood Turner also records a case in which there was
a presystolic, alternating with a systolic, bruit at the apex of
the heart, together with occasional thrill, and yet the autopsy
disclosed no mitral stenosis, but aortic incompetency, the right
and posterior cusps of the valve being chiefly affected. In
another case mentioned by Dr. Turner a presystolic murmur
and thrill were perceptible at the apex, as well as a diastolic at
the base; here the aortic valves were thickened, though there
was uo patency (it would seem most probable that there
was, nevertheless, some regurgitation during life), and the
curtains of the mitral valve were thickened and rough at their
margins, though apparently competent. In a third case there
were soft diastolic, presystolic, and systolic bruits at the apex,

* Cf. p. 153.

AUSCULTATION.

2V4

with a slight diastolic thrill ; here, as shown by post-mortem
•examination, there were aortic disease with incompetency
and mitral disease with incompetency, but no stenosis. Dr.
Turner does not consider that in any of these cases the
murmur, which resembled that of mitral stenosis, was really
one of aortic regurgitation, but adduces them to sustain his
argument against the auricular causation of the presystolic
murmur (St. Thomas's Hospital Reports, 1S76). Dr. Hayden
mentions a case in which the murmur of aortic reflux simu-
lated that of mitral stenosis (" Diseases of Heart and Aorta,"
p. 907). It is a significant fact that in almost every case in
which a presystolic murmur has been recorded, and the
<liagnosis of mitral stenosis has not been justified by the
autopsy, tbere has been either a diastolic murmur heard
during life in some part of the aortic area, or else the con-
dition of aortic regurgitation has been demonstrated by the
post-mortem appearances.

To differentiate between the two conditions, therefore, aid
must be called in from other sources than auscultation. The
existence of hypertrophy of the left ventricle may be shown
by the other signs, and thus the diagnosis will tend to that of
aortic regurgitation ; but the most important evidence is
offered by the sphygmograph and cardiograph (see Part II.).
If under such circumstances the diagnosis between the two
affections be difficult, the determination of the question of
coexistence of the murmurs of aortic reflux and mitral
obstruction may be still more difficult. We shall return to
the question when we consider combined murmurs.

In the case of the murmur occupying tbe whole interval
between second and first sounds, due to mitral stenosis, I can
have no doubt that the early portions of such bruit may be
due to the tension in the pulmonary veins and left ventricle,
unaided by the systole of the latter. That such could be
the case was held by Dr. Wilks. Dr. Galabin came to the
like conclusion from cardiography evidence. The crucial
proof of the truth of the proposition is, I consider, furnished
by cardiograms taken in cases in which I have found a
presystolic murmur to occupy a considerable portion of the
diastolic period, and yet the auricular systole is shown to
occupy only its usual position just before the systole of the
ventricle (see Part II.).

AUSCULTATION.

III. A murmur starting after the second sound and ceasing
with the first sound is distinctly louder at a certain period
in its course. This exaltation of the murmur is indicated by
the swelling in the shaded portion of the diagram, which
resembles one that was figured by Dr. Gairdner in his early
exposition of the presystolic murmur. I have no doubt that
this reinforcement is due to the systole of the auricle, which,
owing to the obstruction at the mitral aperture, takes place
out of the usual rhythm. I shall discuss the evidence which
I believe to fully prove that such abnormal action of the
auricle can, and does, take place in the section on the graphic
signs of mitral stenosis (Part EL ).

IV. A murmur occupies a short interval just before the
first sound, which abruptly terminates it. This is a common
type of presystolic murmurs, and is due chiefly or wholly to
the communicated impetus of the auricular systole (see
Part II. p. 272).

V. A murmur is affixed to the second sound, but ceases
before the commencement of the first sound. Such murmur
has been described by some observers as diastolic, by others
as post-diastolic. The strictly diastolic form of murmurgenerated
at the mitral orifice is very rare. Dr. Hayden states that he has
not met with an example, but mentions a case under the care
of Dr. Stokes in which it existed together with a systolic
murmur. I have recorded a similar case, with what I con-
sider to be the explanation of the phenomenon in that instance.
Dr. Fagge has mentioned cases in which a post-diastolic
murmur of mitral causation ceased before the commencement
of the first sound, and it is quite conceivable that in such the
tension in the left auricle was sufficient to produce a murmur
as soon as the relaxation of the ventricle allowed the flow of
blood to occur into it ; but the muscular feebleness of the
auricle was such that the murmur was not only not prolonged,
but at the later period not even produced. In some rare cases
the two last-mentioned murmurs have been combined : there is
" a murmur of double rhythm, or broken into two fragments,
one of which adheres as a prefix to the first sound, and
represents the ordinary presystolic murmur, whilst the other
succeeds the second sound, being appended to it as a suffix ;
these two fragments being separated by a brief period of
silence "(Dr. Hayden).

AUSCULTATION.

215

We may now briefly consider combined murmurs.
We have already discussed double murmurs — that is to
say, murmurs generated at different periods of the
heart's rhythm at one orifice : by " combined" mur-
murs I mean those which take their origin from more,
than one of the orifices. The following- may be taken
as probably representing the relative frequency of the
combinations : —

(1.) Mitral regurgitation and aortic obstruction.

(2.) Mitral regurgitation and aortic regurgita-
tion, or mitral regurgitation and aortic obstruction
and regurgitation.

(3.) Mitral obstruction and aortic regurgitation, or
mitral obstruction and regurgitation and aortic ob-
struction and regurgitation.

(4.) Mitral obstruction and regurgitation with tri-
cuspid obstruction.

(5.) Mitral obstruction and regurgitation with tri-
cuspid obstruction and regurgitation.

(6.) Aortic obstruction and pulmonic obstruction.*

None of these combinations require particular com-
ment from the point of view of diagnosis, except the
third. You will distinguish them by the rules
already laid down for the diagnosis of the individual
affections. In all cases notice : 1. The positions of
maximum intensity of any murmurs heard over the
cardiac area. 2. Any differences of pitch and cha-
racter. 3. The directions in which the sound is
conveved.

There may be considerable difficulty in determining

* The combination of mitral regurgitation and tricuspid
regurgitation, or mitral obstruction and tricuspid regurgitation,
is a very common one, but very frequently the tricuspid lesion
is not betrayed by murmur.

!316

AUSCULTATION.

the co-existence of aortic insufficiency and mitral nar-
rowing-. A prolonged diastolic murmur may drown
the presystolic. In carrying the stethoscope, how-
ever, down the left border of the sternum you may
probably arrive at a spot where the diastolic murmur
ceases to be audible, and then as you approach the
apex, a presystolic of different pitch and character
may become manifest. The presence of a presystolic
thrill at the apex may aid the diagnosis.

Even though the ordinary means of diagnosis be used with
all care, the question whether or no a mitral direct co-exists
with an aortic regurgitant murmur may be difficult to deter-
mine. Witness the following cases under my care :— 1. A
man of fifty-one, in whom was diagnosed, from the physical
signs, obstruction and regurgitation both at mitral and aortic
orifice. There was no doubt concerning the signs of aortic
obstruction and regurgitation; in addition, there was "a
rolling presystolic murmur two inches below and an inch
outside the nipple, this murmur terminating in a blowing sys-
tolic bruit conducted to axilla." The sphygmographic signs
were typically those of aortic reflux. 2. Alice B., aortic
diastolic murmur with presystolic murmur presenting usual
characters. Sphygmographic signs of free aortic reflux.
Cardiograph shows no sign of mitral stenosis. 3. H. M., low-
pitched murmur with first sound at aortic cartilage ; second
sound murmur left of sternum ; rolling typical presystolic
murmur at apex. Cardiograph shows much hypertrophy of
left ventricle, but no sign whatever of mitral stenosis.
4. Walter F., aged twenty, murmur at first heard in
mitral area, commencing very shortly after second sound, and
after augmenting in intensity, ceasing abruptly with first
sound ; in fact, closely resembling murmur of mitral stenosis.
Coarse thrill also felt at apex. Afterwards, murmur heard to
be diastolic down left border of sternum, but still typically
presystolic at apex. Cardiographic and sphygmographic
evidence indicated free aortic regurgitation, but no sign of
mitral stenosis.

T cannot think that in any of these cases, though there was
a murmur which, in the absence of aortic regurgitation, I
should have considered pathognomonic of mitral stenosis.

A US C .IT I/TiA X I O N .

217

there was any other valvular lesion than aortic insufficiency.
My belief is, as I have before indicated, that the murmur of
-aortic reflux may so closely simulate that of mitral obstruc-
tion as to be absolutely indistinguishable from it. It follows
that if you meet with a case in which, from the co-existence of
the signs of the two conditions, you are inclined to make a
diagnosis of the two lesions, it is right that you should
hesitate and consider all the available evidence. Several of
the cases which have been adduced as telling against the
■auricular causation of the presystolic murmur have been
where the signs of aortic reflux have been undoubted. Now the
combination of mitral stenosis and aortic regurgitation, as
shown by post-mortem records, is a rare one; that of mitral
regurgitation with aortic regurgitation being much more
common. In my belief, the presystolic murmur heard in
aortic regurgitation does not invalidate the auricular hypo-
thesis, but, as I have said' the physical conditions are so
analogous that the sonorous results may be identical. The
<]uasi-presystolic murmur of aortic regurgitation is the con-
cluding portion of a diastolic murmur heard at the apex ; if
the tension is great in the aorta, at the end of diastole, the
murmur is generated with equivalent force to that exer-
cised by the auricle in the mitral lesion ; moreover, the back-
ward flow is capable of generating thrill, which, being most
evident at the later periods of diastole, seems to be presystolic.

I have never met with a case of co-existent mitral
and tricuspid stenosis, but Dr. Hayden, of Dublin,
has recorded three such examples. The presence of
tricuspid stenosis is to be suspected whenever a pre-
systolic murmur is heard close to the left edge of the
sternum. Dr. Hayden " would regard the existence
of two centres of presystolic murmur, with or without
fremitus — viz., at the apex and somewhat to the
right of that situation, in conjunction with marked
systemic venous engorgement — as evidence of the
•double lesion of mitral and tricuspid stenosis."* I

* "The Diseases of the Heart and of the Aorta," by Thomas
Hayden, &c. &c. (Dublin : Fannin & Co., 1875), p. 238.

AUSCULTATION.

had one case which seemed to present this com-
bination, hut the murmur simulating- that of tricuspid
stenosis was found to be due to a rough patch of
pericardium over the right auricle. The probabilities
of tricuspid stenosis were great, for there was very
marked presystolic pulsation in the veins of the neck.
There was tricuspid regurgitation.

The diagnosis of complex pathological conditions
of the heart sometimes presents very considerable
difficulties, and requires great care and repeated ex-
aminations. I would venture to give you one or two
rules to observe when you meet with a difficult case.

In the first place, do not be content to write in
your notes, " rhythm of the heart irregular and
tumultuous," but let there be order in your record of
such irregularity, and system in your treatment of
the seeming chaos.

Record all the signs which you have observed
previously to those derived from auscultation.

Describe the sounds, normal and abnormal, heard
over the situations of each of the orifices.

Note, first, the characters of first sound and second
sound at the aortic cartilage. Reduce these to dia-
grammatic form (see p. 197 et seq.), indicating-
murmurs where present.

Repeat the process at the pulmonary, tricuspid
ind mitral areas successively.

Compare the observations and diagrams only after
they have been completed, and then fill in the lines
of conduction of normal and abnormal sounds (see
p. 83).

Do not unduly hasten to form your conclusions, but
obtain all the evidence possible before you give your
verdict.

PART II.

THE SPHYGMOGRAPH

AND CARDIOGRAPH.

PAST II.

THE USE OF THE SPHYGMQGEAPH AND CARDIO-
GRAPH IN THE DIAGNOSIS OF DISEASES OF
THE HEART.

Invention of the Sphygmograpli— Illustrations of its usefulness

— Varieties of instruments— Mahomed's Sphygmograpli

Pond's Sphygmograpli— Galabin's Cardiograph.

The sphygmograpli is an instrument for enabling- the
movements of an artery which constitute the pulse to
be automatically recorded j the term cardiograph is
used for an appliance which writes the motions of the
heart itself. The idea of making the pulse register its.
own movements dates from long-past ages: it i&
said to have occurred to Galileo. Anything like perfec-
tion in the mechanism adopted has, however, only been
obtained in recent years, when Marey devoted himself
to the investigation of the phenomena of movement in
the vital functions. His sphygmograph is the model
cm which other instruments have been constructed
The mechanical difficulties of record being for the most
part overcome, there remain difficulties of interpreta-
tion—the pulse writes its own hieroglyphics, but these
have to be expounded. The interpreter obtains the key
by patient observation and by experiment. One advan
tageof the evidence obtained by such mechanical mean,
is that, whilst the impressions we have gained by the

THE SPHYGMOGHAl'H.

methods of physical investigation hitherto considered
— whether those derived from our sight, touch, or
hearing- — may fade into the haze of half-forgotten
memories, the story which the pulse writes of itself is
;• permanent. " Litera scripta manet."* You may pon-
der over the record, solve its intricacies at your leisure,
and compare the evidence obtained at one time with
that procured at another. But the question is asked,
Are these practical instruments of diagnosis ? If by
diagnosis we mean not merely the detection of definite
diseases, but the estimation of the degree of deviation
from standard health, undoubtedly they are. Is the
value of the indications which they give commensurate
with the trouble which must be taken to employ them ?
Under present circumstances, certainly. Thanks to
the ingenuity of physicians who are also mechanicians,
the difliculties are so far overcome that the instru-
ments may be used with very little expenditure of time;
they are of daily employment, and every day gives
evidence of their value and importance. They should
be used, however, after the other means of diagnosis,
not before. As Dr. Mahomed has said, they open up
no " royal road to diagnosis," but they may check,
confirm, or extend the diagnosis already attained, and
often throw a new light upon a difficult position. I
may illustrate the value of the sphygmograph by two
examples. I was called hurriedly to a patient whom I
found in the extremities of cardiac dyspnoea. She was
unable to lie down ; there was extensive oedema, and
a loud systolic murmur was heard at the apex of the
heart, conducted towards the axilla and audible at the

* ' ' Segnius irritant animos demissa per aures

Quam quae sunt ocmlis subjecta iidelibus." — Horace, Satires.

THE SPHYOMOQRA PH.

back. I had no doubt that the condition was that of
mitral regurgitation. There was, however, in addition,
extreme anaemia, with hsemic murmurs at the base of
the heart and over the vessels of the neck, and it was
probable that this had been brought about by excessive
haemorrhage caused by uterine fibroid. The question
which now presented itself was — Is this cardiac dys-
pnoea with mitral regurgitation due to organic disease
of the valve, or is it the result of weakness of the muscle
of the ventricle ? Against the first view was the fact
that there had been no rheumatism, acute nor subacute.
On looking at the pulse-tracing, which I had at once
■obtained, I was struck with the fact that it so nearly
approached the normal ; I concluded, therefore, that
the imperfection of the mitral orifice was not the result
of valvular disease. This diagnosis proved correct, for
after treatment the whole of the cardiac signs and
symptoms passed away, and no trace of the murmur at
the apex remained. Another instance. I was called
in consultation with a medical friend to the case of a
gentleman, past middle-age, who in appearance was
hale and well-nourished, and who, it was well known,
had led a careful, abstemious life. The signs were
those of a limited pneumonia of the base of the right
lung. The general conditions did not suggest a bad
prognosis, the only reason in favour of which was the
asserted debility of the patient on attempted movement,
even while in bed ; an expression which seemed not to
be corroborated by the appearances. To the finger
the pulse showed a fair regularity. The sphygmogra-
phic trace, however, gave a different lesson ; though
there was fair regularity in time, there were such
variations in volume and in general characters that I
feared the heart>fibres were degenerated. The prognosis

224

mahomed's sphyomograph.

founded on this observation was gloomy, and the pro-
babilities which were then sketched out were exactlv
confirmed by the facts. The signs of pneumonia passed
away, and it appeared that there' might be a good
recovery; then ensued a sudden syncope and a situation
of grave peril. From this there was a rally and a
renewed hope of recovery ; syncope, however, in spite
of the most watchful care and abundant nourishment,
recurred, and the patient died. These two instances
are, I think, sufficient to show- the value of the sphygmo-
graph as an instrument of diagnosis : in the one case
I consider that it determined the difficult question
whether there was organic disease of the mitral valve or
passive yielding of the ventricular walls ; in the other
it demonstrated an unsuspected condition of degene-
ration of the muscular fibres of the heart. I propose
now to examine more systematically its application and
its uses in the diagnosis of cardiac diseases.

Varieties , of Instruments.— I have said that
these are chiefly founded upon the model of Marey. The
modification of Marey's sphygmograph usually em-
ployed in this country is that designed by Dr. Mahomed.

Mahomed's sphyrjvwgrajM (Fig. 10) consists essen-
tially of a framework containing an arrangement of
levers adaptable to the pulsating vessel. Contact
with the artery, the radial being usually chosen
for convenience, s made by a steel mainspring,
the movements of which, consentaneous with those
of the artery on which it is made to rest, are
communicated to a lever of the third order, so that
the slight motion may be. much amplified (about
ninety times). The writing lever consists of a fine
slip of very light wood, and is so .guarded as to
allow vertical without lateral movement. The motions

mahomed's sphygmograph. 225

of the pulse are thus converted into up-and-down
strokes of the free extremity of the lever ; these are
made to impinge upon a slide, which, by means of
clockwork, is caused to travel at a known rate — about

four inches in ten seconds. Thus the movements of
the free extremity of the lever, representing the
amplified movements of the pulse, are described upon
the travelling slide in a series of figures. For a

220

POND'S SPH YGMOGRAPII.

minute description of the instrument I must refer you
to Dr. Mahomed's paper {Medical Times and Gazette,
January 20, 1872, p. 03).

An essential point is to be able to apply the main-
spring- to the artery with definite degrees of pressure.
This object Dr. Mahomed has attained with great
success. By a very ingenious arrangement the pres-
sure can be increased by turning a thumb-screw, and
this pressure is registered in ounces (1 to 18 troy)
upon a dial-plate.

Pond's Spkygmograph (Fig. 11), which is also adapted
for use as a cardiograph, has the great merit that it
is very readily applied, and its application consumes
so little time that it may be used in daily practice.
I believe that every practitioner, however busy, would
be able to employ it, and would find its indications of
the greatest possible service. In this instrument the
slide of paper or of mica on which the tracing' is
taken, instead of being vertical as in the other instru-
ments, is horizontal, so that the operator looks down
upon it. The throbbings of the pulse are communi-
cated to an india-rubber diaphragm, or, by a late
improvement of the instrument, to a vertical lever
terminating below in a small metal button, and kept
in constant contact with the artery by a spiral spring.
A very ingenious, yet simple, arrangement of levers
causes amplification of the movements which are
recorded on the slide, which, as in the other instru-
ments, travels by clockwork (about six inches in
fifteen seconds). The upright stem of the instru-
ment is provided with a pressure-gauge graduated
from one to sixteen ounces, so that various degrees
of compression can be exerted upon the artery

The sphygmographs of Marey and Mahomed have

pond's sphygmogrAph.

227

been used for taking tracings directly over the heart's
impulse, but, in many cases with these instruments,
the task is impossible — first, because with a strQngly-
acting heart the range of motion, amplified as it is
by the sphygmograph, is too great to be recorded on'

Fig. 1 1.

Pond's Sphygmograph and Cardiograph.

the travelling slide ; and secondly, because the mecha-
nical arrangement adapted to the limited area of a
pulsating artery is ill fitted for fixing over the chest-
wall at the site of the heart's impulse. Marey first
overcame the difficulties, and laid the foundation for

228

galabin's cardiograph.

the study of the movements of the heart by the-
graphic method, by constructing a cardiograph in
which the cardiac motion of the chest-wall was
transmitted to a drum or tympanum, communi-
cating by a flexible india-rubber tube with a second
tympanum, the two tympana, and the tube which
connected them, forming an air-tight cavity. Thus
the motion imparted was transmitted by the oscilla-
tions of the column of contained air ; it was ampli-
fied by a lever attached to the second tympanum, and
recorded on a revolving cylinder termed a polygraph.
Many observations of the highest importance were
made by means of this instrument, but it is now super-
seded by a modification of the sph}rgmograph adapted
to the chest-wall.

Galabin's Cardiograph is that generally
adopted in this country. Its general construction is
that of a magnified sphygmograph, with adjustments
for its adaptation to the thorax. Instead of the rigid
parallel bars of the sphygmograph, the base is consti-
tuted by moveable wooden blocks, which can be
separated to a width of nearly five inches; by means
of these the instrument is made to rest upon the
chest. Between them, by two transverse steel rods,
the brass frame of the cardiograph is supported, and
is attached, by joints which allow of both vertical
and horizontal adjustment, to four vertical rods. It is
possible, therefore, for the instrument to be applied
to a chest of any size or shape. The brass frame
differs from that of the sphygmograph in that the
bar attached to the main-spring has an arrangement
for its elongation and variation of position, so that
the vertical height of the curve described by the
recording style can be varied from 10 to about 10O

galabin's cardiograph*

times the actual movement of the chest-wall.
The mechanism for an exact determination of the
pressure exerted by the main-spring- is unnecessary
in the cardiograph, but there is an adjustment for
reducing this pressure to nearly zero, so that very
slight impulses — even the back-stroke in veins — may
be recorded. (For Dr. Galabin's description vide
« Med. Chir. Trans.," vol. lviii. p. 353.)

SPHYGMOGRAPHIC TRACINGS.

II,

Method of obtaining a sphygmographic tracing with Ma-
homed's sphygmograph — Importance of recording the
pressure employed— Tracings with Pond's sphygmograph—
Cardiographic tracings with Galabin's cardiograph— With
Pond's instrument — Varnishing tracings for preservation —
To multiply copies of tracings.

How to obtain a tracing — (1) with Mahomed's Sphygmo-
graphi — The arm of a patient from whose radial artery
a tracing- is to be taken must be placed upon a splint
or rest, the palm being- upwards. The stand of the
instrument is then applied over the arm in the
longitudinal direction, so that the ivory pad of the
mainspring is just over the artery as the latter lies on
the inner side of the styloid process of the radius, and
is crossing the anterior ligament of the wrist-joint.
In this position the instrument is firmly maintained
by strong bands passing over each extremity of the
framework. The hand is to be bent slightly back-
wards, and may be made to gently grasp a band
stretched across the end of the splint or pad. If the
wrist be strongly extended backwards, the parts are
too tightly stretched and the artery rendered tense
if the hand be firmly closed, the tendons of the
muscles are tightened and made to interfere with the
perfect application of the instrument, or, perhaps, to
produce vibrations in the tracing. The instrument
being applied with these precautions, the artery will
now lie between the ivory rods, and the pressure of
the spring upon it must now be varied (by the operator

SriIYGMOGItAPHIC TRACINGS.

231

turning- the graduated thumb-screw) until the maxi-
mum range of movement of the recording lever is
attained. The il slip" upon which the tracing is to be
taken is now placed on the travelling slide. This
slip is generally of white paper, which should be well
glazed on both sides, so that friction is reduced: to a
minimum. The style of the recording lever may be
supplied with ink, so that it writes upon the white
paper as the clockwork arrangement causes it to
travel along ; this method, however, is often tire-
some, the pen refusing to'mark or the ink being jerked
into unsuitable places. The best plan appears to be
to allow the point of the style to make its mark
upon the paper-slip, which has been previously smoked.
In order to smoke the slip it is only necessary to hold
for a brief period the paper over a small piece of
burning camphor, a kindled pledget of cotton soaked in
olive oil, or a smoking paraffin lamp : by either of these
methods a uniform layer of black is obtained over the
surface of the paper, and, of course, the end of the
writing-lever makes, by displacing the smoke, a series
of white markings as it moves over the surface. The
blackened slip being introduced, and the clock move-
ment wound up, a touch of the button is made to
liberate the spring-, and the slide commences to travel.
It may be stopped at any time, and then the pressure
varied. The most perfect tracing is that in which,
the spring following most perfectly the expansion of
the artery, the summit is most sharply defined (i.e.
free from rounding) and the various notches best
marked. Dr. Mahomed says : " The use of incorrect
pressure is perhaps the most common source of error
in sphygmography, and the greatest care is necessary
in deciding upon the amount of pressure to be

232

SPHYGMOGHAPHIC TRACINGS.

employed. This, when ascertained, should he care-
fully recorded, as it is one of the most important
characters of the pulse. Notice should also betaken of
the amount of pressure required to totally extinguish
the pulse, so that the lever remains perfectly motion-
less ; for by this means an estimate can be formed of
the force with which the heart is contracting."* A
number of tracings can of course be taken at one
sitting : they may be at once examined with care lest
manipulation rub off the coating of smoke. The
name of the patient, &c, the pressure employed, with
a brief note of physical signs, should then be inscribed,
a needle or finely pointed steel pen being used for
this purpose, and each slip be varnished for preser-
vation.

(2.) Tracings with Pond's Bphygmograjili are thus ob-
tained. It is not necessary to use a pad or splint, but
a metallic wrist-rest is supplied with the instrument ;
this is ingeniously constructed, so that it adapts itself
to an arm of any size with no discomfort to the patient.
Tracings may, however, be taken even without the
wrist-rest. An upright bar is inserted into this sup-
port, to which is clamped a transverse arm, which clips
the body of the sphygmograph ; this arm is provided
with a screw adaptation to all necessary positions.
The patient being in the sitting or recumbent posture,
and quite at ease, the hand rests with palm upper-
most; then — the slip of smoked paper or mica having
been introduced by momentarily setting free the watch
movement, allowing the slip to travel for about a
quarter of an inch, and then stopping again — the
operator, holding the sphygmograph by the cylinder,

* Medical Times and Gazette, Jan. 20, 1872, p. 64.

SPHYGM0GRAPH1C TRACINGS.

233

applies the india-rubber base over the pulsating artery.
Due contact between the upright bar immediately in
relation with the india-rubber diaphragm, and the
system of writing levers must now be made by suffi-
ciently turning the small screw at the summit of the
cylinder. The writing-needle will now be observed
to move over the blackened slide. By slightly vary-
ing the position of the india-rubber base over the
artery, and by increasing or decreasing the firmness
of application of the instrument (this pressure be-
ing determined by noting the pressure-gauge), the
point of maximum movement of the needle will be
observed. If the attachment to the wrist-rest be em-
ployed, the instrument should be fixed in the position
at which this maximum of movement is attained ;
but with a little practice the operator will be able to
retain the sphygmograph with uniform pressure upon
the artery, and to dispense, with the clamp which fixes
to the wrist-rest. Then the watch movement is libe-
rated by a touch of the finger, and the slide travels.
Several tracings should be taken at varying pressures.
It is very easy to obtain tracings with this instrument
from the carotids, the temporal arteries, the femorals,
<fc,c, as well as the radials.

I consider it best, when using Pond's instrument, to take the
first slip with gradually increasing pressures every three or
four pulses. Commence with the lowest possible pressure
that will develop the tracing, then stop the travelling of the
slide, and start it again, using slightly increased pressure ;
observe whether increasing pressures increase the altitude and
development. Note the pressure which gives the maximum,
and the effect of higher pressures on the elements of the trace.
Often one slip suffices, but it may be necessary to take two or
three. Thus you are iuformed at what pressure you have the
best tracing, and can proceed to take others at this, which
gives you the most typical results.

834

•CARDIOQBAPHIC TRACINGS.

• (3.) Cardiog-rnphic tracing's may be thus obtained
with QalabivSs Cardiograph. The patient being- stripped
to the waist, the position of the apex-beat should be
determined and marked upon the chest-wall by means
of a pencil. The pad of the lever is then to be ap-
plied over the point of pulsation, and the instrument
adapted by separating- to greater or less degree the
wooden blocks constituting the base, as well as by
altering the position of the instrument in relation to
the vertical rods until it rests suitably upon the chest.
It may be fixed by two partially elastic straps passed
round the body and fastened by buckles. In many
instances it suffices to hold the instrument against
the chest with the hand, the straps, <fcc, being dis-
pensed with. The movements of the recording style
being observed to be in suitable position upon the
smoked paper, the clockwork is started and the tracing-
taken. In some cases the movements of respira-
tion do not greatly disturb the position of the style,
and the series of tracings is well comprised within the
slide. Often, however, the movement of breathing-
causes too great excursion of the style, and the patient,
must be asked to hold the breath — the clockwork
being started at the moment of arrest at the end of
expiration. The position of the patient should be as
much as possible one of ease : if the apex-beat be
fairly defined, it should be that of as complete recum-
bency as is consistent with comfort ; if the apex-beat
be ill-defined, a better tracing may be taken if the
patient be in a sitting position, leaning somewhat
forwards.

(4.) Cardiac tracings with Pond's instrument are
often obtained with great ease. The preliminary
arrangements having been made as when it is used

CARDIOURAPHIC TRACINGS.

235

as a sphygmograph, the instrument is simply held
against the chest-wall at the point of pulsation, and
the clockwork started. To obtain a satisfactory
tracing- it is usually necessary for the patient to be
recumbent; but it is possible to obtain one in the
sitting and even standing posture. The sphygmo-
graph is held by the cylinder or by the barrel of the
watch movement ; the difficulty is, that the needle shall
not by the force of gravity fly off the smoked surface j
sometimes this difficulty may be obviated by removing-
the little weight which serves as a counterpoise to the
needle, sometimes also by bending the needle itself.
It is very important that there should be facility for
taking tracings not only in the sitting- position, but
even when the patient leans well forward.

To preserve sphygmographic and cardiography
tracings they must be varnished. Before this is done,
upon each tracing should be inscribed the name and
age of the patient, and a brief note of the physical signs
or the diagnosis arrived at by the hitherto employed
means. This is easily done by writing on the smoked
surface with the point of a pin or a needle fixed into a
convenient handle. The tracing should then be care-
fully dipped in a rapidly drying varnish. The varnish
may be composed of gum benzoin and methylated
spirit (one ounce of the former to six ounces of the
latter). The following is Pond's receipt : — Alcohol,
one pint ; gum sandrac, three ounces ; castor-oil, half-
ounce ; mix.

To multiply copies of tracings the original should be
taken on a slip of mica and well varnished. When
quite dry it should be placed in a pressure-frame, such
as used by photographers, with a slip of photo-sensitive
paper behind it, so that the latter becomes printed off

•236

COPIES OF TRACINGS.

as a positive impression from a negative photograph.
A child's transparent slate provided with a clear glass
forms a very efficient pressure-frame. The solution
•with which the paper is rendered sensitive is thus
prepared: — (1.) Ammonio-citrate of iron, 1§ ounce ;
water, 8 ounces. Make a solution. (2.) Redprussiate
•of potash, 1^ ounce ; water, 8 ounces. Dissolve. Mix
the two solutions and keep in the dark or in a yellow
bottle. This solution being poured into a saucer, strips
of white unglazed paper are to be wetted with it on
one side only, and then allowed to dry in the dark
until wanted. The sensitive side of the paper being
■pressed against the negative mica-slip, so that the
tracing reads correctly, it is exposed to sunlight or
daylight for a term varying from twenty minutes to
-two hours according to the intensity of the light.
When removed from the pressure-frame, the paper
must be washed in clear water for a minute or two, and
fthe tracing will appear in blue lines upon a white
ground. If properly managed, the copy is permanent.
It is obvious that copies of many slides may be taken
in one frame at the same time, and by consecutive
-operations almost any number may be procured from
-one mica.

THE PULSE-TRACE. 237"

III.

Interpretation of the normal pulse-trace — The first event, or
percussion wave— The second event, or tidal wave— The
third event, or dicrotic wave — The diastolic portion — Inter-
pretation of the normal heart-trace — The systolic portion—
The diastolic portion— Indications afforded by the sphygmo-
graph — Frequency of pulse — Irregularity in time — Intermit-
tency— Irregularity in volume, rhythmical and arhythmical —
Relation of pulse to respiration— Respiratory line — Undu-
lation of base-line in cerebral diseases.

Interpretation of the normal ptilse-tr ace. — The tracing;
of a single pulsation in a state of health ' consists of
(1) a line which is vertical or nearly so (Fig-, 12, ah)..

Fig. 12.

The normal pulse-trace magnified : a b, percussion up-
stroke; a be, percussion wave; c d e, tidal wave:
d ef dicrotic wave.; at e, aortic notch; fa, diastolic
period. '

The contraction of the left ventricle forcing- the con-
tained volume of blood into the aorta, suddenly dis-

238

the pulse-track;

tends the systemic arteries; the lever, therefore, in
contact with the artery, receives a sudden impulse
which jerks it upwards; the vertical line is the result
of the movement of the vessel thus produced, amplified
by the mechanism of levers and somewhat by acquired
velocity. This, then, is the- first event, an almost in-
stantaneous up-stroke, often termed the percussion-
stroke. Having" attained its maximum height, (2) the
line now begins to descend at an acute angle to the
up-stroke, the sudden force of elevation having been
expended, but again rises at e d, so that it forms a
curve. This is due to the fact that the lever, which
falls by its own weight after the expenditure of its
abruptly-communicated velocity, is again caught and
lifted by the tide of the onward current of blood.
This is the second event, and the wave thus produced
is termed the tidal wave. The line inscribed by the
lever now descends, and again rises, forming a second
curve (ef). This is the third event, the, dicrotic wave. The
curve produced is an important one. It is due to a re-
bound of the blood from the point <£appui constituted by
the cardiac end of the aorta with its closed semilunar
•valves. Marking as it does the closing of the aortic
valves, the notch thus produced is termed the aortic
■notch. So for, therefore, the trace has indicated only
the systolic portion of the cycle ; the brief remainder
comprises the diastolic portion. This consists of the
wave springing from the aortic notch and a gradually
sloping line, ending at the base-line of the tracing.
Its vertical height is about one-third of the percussion
up-stroke. In delicate tracings a very slight elevation
is sometimes seen just as the down-stroke ends and
the up-stroke of the succeeding pulse commences ;
this marks the systole of the auricle.

THE HEAKT-TKACE.

239

Interpretation of the normal heart-trace (Figs. 13 and
14). — As with the sphygmogram, the most promi-
nent feature of the cardiogram is a sudden elevation
denoting- the contraction of the ventricle. Following

Fig. 13.

The normal cardiac trace (after Galabin). A, Typical
apex tracing, a, auricular systole ; a d, ascent due to
Sudden hardening of ventricles ; d e f, continued sys-
tole ; k, rebound after emptying of ventricles ; I, ascent
from gradually increasing influx of blood into ventricles
during diastole. B, Tracing from a healthy man ; tension
low, and heart acting vigorously, g, notch indicating
closure of semilunar valves.

Fig. 14.

Normal cardiac trace (after Pond). The references a
the same as in Fig. 13.

the chief elevation, on the hroad summit of the
trace, however, are one or two waves which have
been said to denote oscillations of the auriculo^

240

SI'HYOMOORAPHIC INDICATIONS.

ventricular valves during- systole. It seems to me-
more probable that they are due to the muscular
movements of the ventricle. At the end of the
elevated portion of the trace is a more rounded
swelling-, which marks the termination of the ven-
tricular systole. The line then descends with a slight
slope to the base-line. Now commences the diastolic
portion of the tracing. In this is seen first an
eminence, which indicates a shock lifting the apex
after the relaxation of the ventricles ; next, a slightly
ascending line, broken by some slight undulations,
marking the time during which the blood-pressure
in the ventricle is increasing ; and lastly, a small
eminence immediately before the succeeding up-stroke,
due to the contraction of the auricle.

It will be seen that the evidence obtained by the
cardiograph is complementary of that afforded by the
sphygmograph. By the latter we obtain a more
complete record of the systole of the ventricle, and
its effect on the peripheral arteries, whilst by the
former we gauge more completely the conditions of
blood-pressure in the ventricle during diastole.

Indications afforded by the Sphygmograph,
— The sphygmograph records the frequency of the
pulse. Care should be taken as regards each instru-
ment to estimate the time which the slide takes to-
travel. This maybe done by a stop-watch, and the mean
of several observations should be taken. Occasion-
ally the process should be repeated with individual
instruments to ascertain whether in course of time the
clockwork alters speed. The instrument is usually so
constructed that six inches travel in fifteen seconds.
To count the pulse, therefore, measure off six inches
of the tracing, and multiply by four the number of

SPHYGMOGRAPHIC INDICATIONS. 241

pulsations observed. This of course gives the rate of
the pulse per minute.

The sphygmograph also records irregularities in time.
It registers intermittency in the pulse (see Figs. 15 and
16). It is obvious that in these cases the heart rests

Fig. 15.

Irregularities in time. Tracings from right radials in
cases in which irregularity disap2>eared after treatment.
(In the upper tracing tension is moderate ; in lower ten-
sion is low.)

Fig. 16.

Intermittency in pulses of high tension.

during the period of a single pulsation, and that this,
intermittency is repeated at intervals. Such irregu-
larities are not uncommon in old persons, or in the
young when convalescent from acute diseases. They
are . usually of no serious prognostic import. Sometimes

242

4 •

sf>HYGMOGRAPHIC INDICATION'S.

the condition is habitual, and uninfluenced by treat-
ment ; in others it is remedied with ease. A change of
dietary sometimes alone suffices ; abstinence from tea,
coffee, or other exciting- beverages, may soon restore
the heart's regularity. In the case of one of my
patients the irregularity entirely ceased after omitting
potatoes as an article of food ; no doubt the error of
excess in this particular had been committed previously.
The indication, however, may be very important ; in
one of my patients the advent of intermittency occurred
in the early stages of the development of cancer of the
liver, when the signs and symptoms were very obscure.

A glance at the sphygmographic tracing shows also
if there be irregularities in volume. These may be
rhythmical or arhytlimical. The most striking example
of rhythmical irregularity of volume (Fig. 17) was in a
case in which there was no cardiac disease, but heini-

Fig. 17.

Rhythmical irregularity in volume in a case of cerebral
disease attended with Cheyne-Stokes dyspnoea. Traces of
right radial artery (5 oz. pressure). A, taken during
period of excitement of respiration ; B, during arrest of
respiration.

plegia, aphasia and the phenomena of Cheyne-Stokes
respiration (see p. 35). The autopsy showed that there
was much cerebral disorganization, the remote effect of

SPHYGMOGRAPHIC INDICATIONS.

243

embolism of some of the cerebral arteries-. In my
opinion, there was in this case a direct disturbance
both of the respiratory and the cardiac centres. The
pulse-tracing- shows that ' each systole of greater is
succeeded by another of lesser amplitude (Fig. 17).*
Another example of double systole (the pulsus
pigeminus) is seen in .a tracing by Dr. Pond (Fig. 18).

J?IG. IS.

Pulsus trigeminus.

Irregularities in volume in which there is no ob-
servance of rhythm as indicated by the sphygmograph
are of high importance both in diagnosis and prognosis.
Here we observe the elevations in succeeding pulsa-
tions to vary very considerably, and in an irregular
manner ; so in the trace the height of the percussion
stroke in one instance may be four times greater than
in others. Arhythmical irregularity in volume may be
demonstrated by the sphygmograph when it is not
detected by the finger. The tracing (Fig. 19)- was
taken from a case in which the finger failed to 'detect
any notable irregularity. This was no doubt due to
the fact that the pulsations were fairly regular in
point of time. The sphygmographic evidence alone
led to the diagnosis of cardiac degeneration.

* Thia has been termed by Traube the. "pulsus alternans."

n 2

SPHYGMOORAPHIC INDICATIONS.

Irregularities in both time and volume are shown
in the acute fevers when the muscle of the heart has

Fig. 19.

Arhythmical irregularity in volume. Tracing from
right radial artery iu a case of pneumonia, with probable

cardiac degeneration.

Fig. 20.

Irregularity in time and, volume (myocarditis in course
of typhoid fever).

been involved in disease (Fig*. 20), as well as in the
later stages of valvular diseases.

Inspection of the sphygmographic trace in series
also indicates the relation of pulse to respiration. The
base-line of a series— that is to say, a line drawn so as
to join the lowest points of the percussion up-strokes—
should be straight. A line so drawn is termed the
respiratory line. If the arterial tension vary, this
line will be not straight but a series of curves. In
health, if a deep inspiration be made during the time
that the sphygmogram is taken the line curves down-
wards, because, owing to the suction-action of the
thorax, general arterial tension is reduced"; on the-

RESPIKATORY LINE.

245

other hand, if a deep expiration be'made, an elevation
takes place in the respiratory line. In cases of dis-
ease in which the rhythm of respiration is disturbed,
this curving or.undulation of the base-line is observed,
and as each curve represents a respiration, the ratio
-of pulse to breathing- is easily ascertained by counting-

-Fig. 21.

Marked undulation of base-line (from a case of
tubercular meningitis).

the number of traces in each curve.* In other cases
there may be seen irregularities in the curves not
corresponding to the obvious rhythm of respiration :
thus one pulse-trace in every two, three, or five, may
descend to the base-line ; this is especially seen in
cases where there are cerebral complications. ("See
Pig. 21.)

* Such a trace is seen in Fig. 25.

246

ABNORMAL PULSE-TRACE.

IV.

Interpretation of the abnormal pulse-trace— Causes of aug-
mented and of lessened percussion wave — Oblique percussion
— Causes of increase and of decrease of tidal wave — Of

dicrotic wave — Estimation of arterial tension— Pulses o^

high and of low tension— Supernumerary vibrations.

Interpretation of the Abnormal Pulse
Trace. The elements which we have considered of the
pulse-trace are all capable of modification under con-
ditions of disease. The percussion-wave is increased

by sudden and forcible contraction of the left ventricle, and
by a large amount of blood distributed by the systole.

Trace showing oblique ascent and descent (tidal wave
only), taken from left radial artery in a case of aneurism
of the left subclavian (Dr. B. Foster).

It is lessened by feeble or gradual contraction of the
ventricle, and by a small amount of blood distributed
by the systole. When the up-stroke deviates from the
vertical line, there is toiling- on the part of the ventricle,
or disease in the coats of the vessel through which the
arterial current flows. In some cases in which the
sphygmograph can be applied directly over the sac of

PULSE-TRACE IN ANEURISM.

•247

an aneurism the tracing* shows only gradually sloping
lines of ascent and descent ; it is thus reduced to its
simplest form, resembling that recorded by the mere
pulsatile injection of fluid into an elastic tube. There
is here only one wave — the tidal ; it is exemplified in
the tracing (Fig. 22) taken from the left radial in a
case of aneurism of the left subclavian artery by Dr.
Balthazar Foster.* The aneurismal sac here acts the
part of a mere elastic bag. In other instances the
modifications are less notable, but a sloping line of
ascent is characteristic (see Fig. 23).

Fig. 23.

Pulse-tracings in cases of aneurism showing obliquity
of percussion-stroke (from left radial arteries in two cases
of aneurism of the arch of the aorta).

Whilst we look upon the percussion as the heart wave
— an indication of the shock communicated by the
grasp of the ventricle upon the contained blood — we
may regard the tidal as essentially the blood wave,
and a measure of the volume projected through the
arteries. The tidal wave is increased by slow contraction
of the ventricle, by a large volume of Mood delivered through-

* " Clinical Medicine" (London, J. and A. Churchill, 1874),

248

ABNORMAL rULSE-TRACE.

out the arteries fa/ the ventricular systole, and by obstruction
in the capillary circulation. On the other hand, it is
diminished by sudden contraction of the ventricle,
by a small quantity of blood delivered, and ~by increased
outflow or free circulation in the capillaries. The
tracing- in cases in which the tidal wave is exaggerated
shows a broad, almost flat, summit ; occasionally the
tidal wave rises higher than the percussion up-stroke
(see Figs. 24 (last tracing) and 47).*

The dicrotic wave is the wave of recoil. The onward
tide of blood having more or less distended the elastic
arterial channels, the sudden closing of the aortic
semilunar valves imposes a barrier against any flow
towards the heart ; the column, therefore, rolls back
towards the periphery and distends a second time the "
arterial channels with this dicrotic wave. The dicrotic
wave is increased by sudden contraction of the ventricle
when the arteries arc imperfectly filled, by increased outflow
or free capillary circulation, and by a relaxed condition of
the 'muscular coat of the arteries. It is decreased by a
gradual systole of the ventricle, by a state of distension
of the arteries, by contraction of the arterial wall
upon its contents, and by obstruction in the capillary
circulation.

To estimate arterial tension. — By high tension in the
arterial system is meant a condition in which the pres-
sure of blood within the arteries is unduly great. The

* The tidal wave should not extend beyond a straight line
drawn from the summit of the percussion up-stroke to the
bottom of the aortic notch. If any portion of the tidal wave
encroach over such line, it is unduly developed. For many
of these observations I am indebted to Dr. Mahomed's
account of the Sphygmograph in Gant's " System of Surgery, "
2nd ed., vol. i.

ARTERIAL TENSION*

249

absolute amount of blood the arteries contain need not
be greater, but may be much less, than normal, but
the artery is tightly contracted on its contents. So
the pulse may be either full, strong and incompressible,
or small and wiry. One important sphygmographic
evidence of increase of tension is the undue prominence
of the tidal wave which Ave have considered, but it is
'a mistake to consider that this sign alone suffices. We

Fig. 24.

Pulses of high tension.

shall presently see that the tidal wave may be pro-
nounced when the tension is low. The concurring
signs necessary for the demonstration of high tension
are — (1) in taking the sphygmogram low degrees
of pressure upon the artery fail to develop the trace,
whilst firmer compression succeeds ; (2) the dicrotic
wave has a position higher than normal in the tracing
and is often but slightly pronounced (Figs. 16 and 24).

Low tension, on the other hand, means imperfect
repletion of the arteries, whose muscular coat is weak

250

DICROTIC PULSE.

or relaxed. It is indicated by undue prominence of
the dicrotic wave. We have seen that the dicrotic
notch is decidedly marked in the normal pulse. In
a sense, therefore, the pulse is dicrotic in health.
The term " dicrotic," however, is usually applied to

Fig. 25.

Pulses of low tension, showing full dicrotism and
hyper-dierotism, (1) from a case of pneumonia which
proved fatal, (2) from a case of typhoid fever which even-
tually recovered.

a pulse in which the aortic notch descends abnor-
mally low. When this notch reaches to the level of
the base-line, the pulse is said to be f ully dicrotic, and
if it sink below this line it is called hyper-dicrotie
(see Fig-. 25). Such signs generally indicate serious
conditions of debility.

In some tracing's the line of descent is broken by
many vibrations. These may be clue to oscillations

Fig. 26.

Extra or supernumerary vibrations (tracing of left
radial in a boy the subject of htemophilia).

ABNORMAL PULSE-TRACE.

251

extrinsic to the artery, but in many cases they arise
in the arterial wall itself. When it is very pro-
nounced in young1 persons, I consider that it may be
taken to indicate an abnormal condition of the arterial
coats (see Fig-. 26). In advanced age the condition is
much more common, and, taken with other signs, indi-
cates arterial degeneration (see some of the tracings
in Fig. 24).

252

CARDIOGRAPH IC INDICATIONS.

V. .

Indications afforded by the Cardiograph — Relation of cardiac
revolutions to rhythm of respiration — Abortive systoles —
Inversion of the trace — Interpretation of the systolic portion
of the abnormal cardiac trace — The up-stroke ; its relation to
the closure of the auriculo-ventricular valves — The summit
and the prominence which terminates it— The down-stroke,
and its relation to the closure of the semilunar valves.

Indications afforded by the Cardiograph. —
Inspection of the heart-tracing1 in series may show the
relation of heart's action to respiration. When the
breath is held the base-line is straight, but when
respiration continues the curves are much more pro-
nounced than is the case with the sphygmogram.
Thus, on inspecting a heart-trace, you may find that
each curve corresponds to from three to seven systoles,
and these may vary much in definition and amplitude.
Such variations and effacement of systoles are some-
times due to the direct intervention of the lung, in
inspiration, between the heart apex and the cardio-
graph lever. Sometimes, this cause being excluded,
the systoles are observed to be irregular or abortive.
Thus, in Pig. 27 there is a systole of small volume
interposed between two of larger, then follows one that
is very small, and succeeding the seventh systole is an
irregular rise not corresponding to a complete cycle.

A difficulty which may beset the interpretation
is inversion of the tracing. The spot at which the
heart's apex impinges in such manner as to produce
bulging outwards of the chest-wall, and consequently

INVERSION OF CARDIAC TRACE.

253

an ascent of the cardiograph lever, may be very
limited. At the moment of systole the muscles of
the ventricles draw themselves inwards towards
this centre of impulse. It follows that unless the
lever be exactly over this spot it may be drawn inwards

Fig. 27.

Irregular and abortive systoles. Cardiogram from a
case of mitral stenosis and regurgitation, with tricuspid
regurgitation. :

with the motion of the ventricular wall, instead of
being- forced outwards at the point of maximum
elongation of the ventricle ; in such case the tracing-;
becomes inverted* A tracing- of this kind may be'
read as a positive if it be turned upside down and
examined from right to left. Or, more simply, a
small mirror, such as that of an ophthalmoscope, may
be placed behind it, and the reflected image read as a,
normal tracing. Sometimes it happens that a tracing-
is partially inverted, and then the difficulties are greater,
and interpretation may be hopeless. In such case,
tracings should be attempted at several situations over
the impulse. Prom inversion of the tracing we are
not justified in making any diagnosis of adherence of
the pericardium as has been supposed.

* Inversion often happens when the maximum of impulse is.
against a rib instead of being in an intercostal space, or where
the heart is covered by emphysematous luncr.

254

ABNORMAL CARDIAC TKACE.

Interpretation of the abnormal cardiae trace. — As
with the sphygmograph trace, so with the cardiac,
each element must he carefully examined. First, the
upstroke. This is increased in vertical height by sud-
denness of ventricular systole, but by no means ne-
cessarily by hypertrophy of the ventricle. In my own
cases the greatest height of up-stroke was attained in
a case of ulcerative endocarditis, in which the valves
of the left chambers became rapidly diseased, and
there were many embolisms. A reference to Fig'. 28
will show how sudden and vertical the up-stroke may

Fig. 28.

Cardiogram in a case of nervous palpitation; no .organic
disease.

become in conditions of palpitation. One of the
loftiest up-strokes in the cardiograms figured by Dr.
Galabin was in a case of exophthalmic goitre — a con-
dition which we know to be associated with the sudden
systole of a feeble ventricle ; with much palpitation, in
fact. In this case there was also mitral regurgitation
(" Guy's Hospital Reports," 1875 ; Plate III. fig. 8).
On the other hand, in cases of considerable hyper-
trophy of the left ventricle, and in aortic regurgitation,
where the jjulsc-trace shows very considerable ampli-
tude, the cardiac up-stroke may have a vertical height
much less than normal. ; ...

ABNORMAL CARDIAC TRACE.

255

The closure of the auriculo-ventricular valves occurs
during the up-stroke. The first sound is heard shortly
after the lever commences to ascend, and its greatest
intensity appears to he at ahout the completion of
two-thirds of the elevation. This point marks the
complete closure of the auriculo-ventricular valves,
and in some tracings it is rendered visihle by a slight

Fig. 29.

Cardiac tracings, showing the prominence h, due to
closure of the auriculo-ventricular valves. A and B, taken
by Galabin's cardiograph, from a case of aortic obstruc-
tion and regurgitation with some mitral regurgitation
6, D , taken by Pond's instrument, C, from a case of
mitral stenosis ; D, from a case of mitral stenosis with
regurgitation and signs of hypertrophy of the left ven-
tncle.

interruption of the up-stroke. This is point I in the
tracings (see Fig. £9). It does not occur when the
systole is sudden. In the cardiograms figured by
Dr. Galabin (" Guv's Hospital Reports," loc. cit.) it is
seen in the hypertrophy accompanying chronic
Bnght's disease, in aortic disease (with regurgita-

256 ABNORMAL CAHBIAC TRACK.

tion), and in mitral stenosis. Of fourteen cases in
which I have found it well marked, ten presented
the signs of mitral stenosis, the others being
instances of aortic disease.

In the next place, observe the summit of the trace.
The extent of this summit is a measure of the duration.
of the systole. When the contraction of the ventricle
is very sudden, there is an immediate fall. A refer-
ence to Fig. 28 will show that this occurs at intervals in
conditions of palpitation, the tracings of intervening
pulsations having broader summits. When, however,
the vertical up-stroke, followed by an immediate, or
almost immediate, down-stroke, is the general cha-
racter of all the individual tracings, feebleness or
dilatation of the ventricle is indicated. I have said that
the undulations which are visible in the horizontal
portion of the summit of the cardiac trace are pro-
bably due to the muscular movements of the ventricle.
In cases of mitral regurgitation, sometimes the broad
summit is formed by a vibratory line, which may be dis-
tinctly traced to the sonorous vibrations of a murmur
(examples are seen in Fig. 42; see also Dr. B.
Foster's " Clinical Medicine," Fig. 18, p. S09).

We have now to consider the termination of the
horizontal portion of the summit in eminence /.
In palpitation, and in cases of the sudden systole of
a dilated ventricle, this eminence may be entirely
lost. On the other hand, in hypertrophy of the left
ventricle it is prominent or rounded* In some cases
the prominence and amplitude of eminence /may be
found to vary considerably in successive systoles.

* I have noticed that the eminence has become markedly-
more rounded after the influence of digitalis.

CLOSURE OF SEMILUNAR VALVES.

257

This I have found to occur chiefly in disease of the
mitral valves, most frequently in stenosis, and in the
douhle lesion of stenosis and regurgitation ; hut I
have also observed it in combined aortic and mitral
disease. I consider prominence of / to indicate
forcible distension of the aorta at the end of ventri-
cular systole.

We have next to consider the dovvnstroke, and
observe whether there is any indication of the
closure of the aortic semilunar valves. Practically,
we may consider that the heart's second sound is
synchronous with the downstroke ; but in some cases
the shock communicated by the reflux of blood
against the valves is rendered perceptible by a notch
or wave (g) in the tracing-. This is usually near the
end of the downstroke, and is here observed espe-
cially in cases in which arterial tension is low. It
will be observed in the normal tracing- (Fig. 13) taken
when tension was low, but it is often very slightly
marked. Dr. Galabin's cardiograms show it in mitral
and in aortic disease. I have seen it in aortic disease
in which there is but slight regurgitation (especially
where obstruction and regurgitation are combined)
and in mitral stenosis. You will observe it low in
the downstroke in Fig. 27, 7th, 8th, 9th, and last
systoles.

L'68 RELATIONS OF SYSTOLE ANT) DIASTOLE.

VI.

Indications afforded by the Cardiograph continued — Relative
duration of systole and diastole — Causes of variations —
Interpretation of the diastolic portion of the abnormal
cardiac trace — Difficulty of interpreting the eminence oc-
curring immediately after the down-stroke— Its relation
to suddenness of systole and suddenness of initial diastole
— Line indicating rise of blood- pressure in the ventricle —
Indication of auricular systole and its significance.

I have said that breadth of the summit of the
trace is a measure of the duration of the systole and an
indication of hypertrophy of the ventricle. This indi-
cation is of more importance when it is considered
relatively to the period of diastole. It is usually held
that | of the cardiac cycle are taken up by the ventri-
cular .systole, and % by the diastole. According to the
estimate of Landois, supposing the whole cycle to last
1-130 second^ the systole occupies -451 second, and
the diastole '679 second* A measurement of the
tracing- of the healthy heart obtained by Galabin's
cardiograph (Fig. 13) shows that whilst the systolic
portion of the cycle occupies if inch linear, the
diastolic portion measures from to if. In the
normal tracing obtained by Pond's instrument (Fig.
14) the systole is measured by about and the
diastole by about of an inch. It is important,
as evidence of a morbid condition, to note any

»Cf. Foster's "Tex1" Book of Physiology," p. 102.
London : Macmillan. 187 7.

RELATIONS OF SYSTOLE AND DIASTOLE. 250

variations from the normal relations of systole and
diastole observed in the cardiography trace. The
diastolic portion of the tracing may be relatively dimi-
nished in hypertrophy, but it is much more manifestly
so m cases in which, in addition to hypertrophy, there is
a condition in existence in which the ventricle becomes
too rapidly filled— such occurs in aortic regurgitation
and in mitral regurgitation, and, & fortiori, in both
combined. The diastolic portion is relatively increased in
the following conditions :-(«) When the heart's action
becomes slow ; « a frequent differs from an infrequent
pulse chiefly by the length of the diastole."* This is
exemplified by a tracing figured by Dr. Galabimf
which was taken from the exposed heart of a do-
when circulation was beginning to foil— the diastolic
interval is greatly prolonged (b) in dilatation of the
ventricle (Galabin, loc. cit, Plate II. Pigs. 14 and 15).
I his may be inferred because the opposite conditions
suggest, as we have seen, hypertrophy. The obser-
vation is of the highest importance as indicating in
valvular lesions a want of compensation (loc. cit,
Plate III Fig 5) .(,) in mitral stenosis. This is often
very maVkedly shown by the cardiograph. The dias-
tolic interval, besides having characters which I shall
presently describe, is greatly prolonged. Thus the
condition may be indicated when it has not been
rendered evident by physical signs, and the proba-
bility of combined stenosis may be shown when there
are physical signs of only mitral regurgitation • so
also may be determined the question of its co-existen "
with aortic disease (cf. p. 210)1 '^ence

i "Guv*, °f Physiol°gy." P- 109.

t Guy s Hospital Rep." 1875, Plate I. pig. 7.

260

THE DIASTOLIC PERIOD.

Again, when the diastolic interval is observed to
vary greatly in duration, as in Fig. 27, there is con-
siderable evidence of an impeded supply to the
ventricle on account of mitral stenosis.

Having considered the diastolic period as a whole,
we will now look more closely into individual charac-
teristics. First point It, the interpretation of which is
undoubtedly difficult. The elevation It is a very
marked feature in the trace, both in health and in
disease. It is clearly established that it is not simul-
taneous with the closure of the semilunar valves, but
occurs subsequently to the second sound. In the trace
it is observed after the downstroke. If we come to
consider the various morbid conditions in which
eminence 7t is either increased or diminished, we find
many difficulties in the way of definite conclusions.
A reference to Fig. 13 might give the impression that
in health it is augmented in a condition of low tension,
but some of Dr. Galabin's cardiograms show that it
may be also greatly

is high, as in hypertrophy of the left ventricle occur-
ring with chronic Bright's disease. I have found it
pronounced in conditions both of high and of low
tension, and in disease of both mitral and aortic
valves, but relatively of greater frequency in mitral
lesions. On the other hand, I have found eminence
k ill-pronounced or absent when the left ventricle
has begun to fail, in the seemingly opposite con-
dition of ventricular strength when there has oeen
aortic disease, and again in the hypertrophy associated
with Bright's disease. I think I may say that an
ill-pronounced eminence h is considerably less com-
mon in mitral regurgitation than is the opposite
condition of exaggeration, excepting in cases wherein

THE DIASTOLIC PERIOD. 261

there are signs of failure of cardiac power or the
heart's action is notably slow.

Dr. Galabin considers that eminence Jc, though not
synchronous with the closure of the aortic valves, is
due to a reflux of blood against the valves— an
explanation to me difficult to accept, when we con-
sider that it is by no means constantly related with
increased blood-pressure in the aorta, and often is
associated with an opposite condition.

Dr. Foster considers the eminence due to the first
influx of blood into the ventricular cavity ; and this
would seem feasible, as it immediately follows the
lowest point of the downstroke — i.e., the maximum
relaxation of the ventricle. Dr. Galabin objects that
if so the elevation would not be followed by so marked
a fall, an objection which does not seem to me fatal,
because the entry of blood, being sudden, might pro-
duce the effect of a vibration. The frecpient want of
relation, however, between the magnitude of k, and
the conditions which would increase the volume and
momentum of blood entering the ventricle, are serious
objections to Dr. Foster's theory. The condition
which I consider to be the most constantly related
with the development of eminence ft, is suddenness in
the action of the ventricle. Thus a reference to the
•cardiogram taken during palpitation (Fig. 28) will
show that those systoles in which there is a high
systolic rise and rapid fall, are immediately succeeded
by a lofty eminence k, whilst the intervening cycles
show a more flat diastolic period. Again?, in the
normal tracing (Fig. 14) the more vertical downstroke
is followed by the more pronounced eminence ft. On
the other hand, the sloping downstrokes indicating a
more gradual unfolding of the ventricle in

THE DIASTOLIC PERIOD.

are followed by only a slight or imperceptible
eminence It. Suddenness of action of the ventricle,
and especially of diastolic relaxation, appears, there-
fore, to me to be the most probable cause of a
high development of eminence k. Thus I think
can be explained its magnitude in conditions of
both low and high tension — in low tension when
there is rapid systole and sudden relaxation of the
ventricle followed by slight recoil ; in high tension
and ventricular hypertrophy when the diastole may
be expedited by the sudden and forcible entry of blood
through the coronary arteries into the heart- muscle.
On the other hand, when from any cause there is
slow or gradual relaxation of the ventricle, eminence
It is ill-pronounced.

Of less difficulty is the explanation of the condition,
when eminence It is lost or merged in the elevation
intervening between the downstroke and the up-
stroke of the following systole. This is well exempli-
fied in Fig. 31. It indicates rapid impletion of either
of the ventricles or both ; it is seen in mitral regurgi-
tation, especially when co-existing- with tricuspid or
with aortic regurgitation.

We turn next to line I, which is an indication of
the filling of the cavity of the ventricle. Here, also,
there is no room for doubt ; the degree of ascent of
the line is a measure of the degree of blood-pressure
in the ventricle. If you compare Fig. 30, taken in a
rase of mitral regurgitation, with the healthy trace,
Fig-. 14, you will find that but little difference is
obvious in the general characters; but the diastolic line,
i nstead of being nearly horizontal, ascends progressively
to the junction with the systolic. This, with a little
broadening of the systolic portion, is the only point of

THE DIASTOLIC PERIOD.

203

dissimilarity. These points suggest that the regurgi-
tation causes a greater blood-pressure in the ventricle
during the diastolic interval than in health, and there
is compensatory hypertrophy. From this, in which the
indication is but slight, turn to Fig. 31, in which you
observe after eminence It a rapid and very marked

Fig. 30.

Cardiogram from a case presenting a soft systolic mur-
mur at the apex, and a history of rheumatic fever three
years ago, showing the line indicating the blood-pressure
in the ventricle during diastole to ascend slightly. Com-
pare with line I, in normal diastolic period, Fig. 14.

Fig. 31.

\ i \ ■

v»uuUSuui i om a case oi aortic regurgitation and ob-
struction combined with mitral regivrgitation, showing
marked ascent of the line iudicatmg intra ventSa?
pressure durmg diastole. h >entriciuar

ascent-here the ventricle is filled, not gradually as
in health, but by a rapid influx both from the aorta
and from the left auricle, owing to the insufficiency of
both aortic and mitral valves. The progressive and

264

PRESYSTOLIC VIBRATIONS.

rapid rise of line I is chiefly seen in mitral regurgita-
tion or aortic regurgitation, and especially when these
lesions are combined ; but it may be seen also in
mitral stenosis, and then is an indication of con-
siderable hypertrophy (compensatory) of the left
auricle. More commonly, in mitral stenosis, the line of
ascent I varies considerably in different cycles. This
is well seen in Fig. 32, in which there is regurgila-

Fig. 32.

Cardiogram in a case presenting variable systolic and
presystolic murmurs, showing variations both in systoles
and diastoles.

Fig. 33.

Cardiogram in a case of mitral stenosis, showing
vibrations in diastolic period corresponding to presystolic
murmur and thrill.

tion as well as obstruction ; some of the diastolic
intervals present only a sudden rise and fall, whilst
others show a serrated line, which we shall consider
as denoting the sonorous vibrations of a presystolic
murmur, or the vibrations, sensible to the touch, of a
thrill. The latter is also seen in a very marked

AURICULAR SYSTOLE.

265

manner in Fig-. 33. A great variation in the con-
ditions of blood-pressure in the ventricle is also seen
in Fig. 27, where tricuspid regurgitation existed as
well as mitral regurgitation and stenosis.

We have next to consider the eminence a, which in
the normal trace we have no difficulty in ascribing-
to the auricular systole; When this eminence is
exaggerated, we have evidence of auricular hyper-
trophy. This is well illustrated in the two cardio-
grams of Fig. 34. It might be considered d priori
probable that, inasmuch as in mitral stenosis the left
auricle is usually considerably hypertrophied, the

Fig. 34.

Mriri? a t.l 8 i m^1Ca*1rnf ^'trophy of the left
auricle. A taken by Dr. Mahomed from point of apex-
beat by ordinary sphygmograph in a case of great hyper-
trophy of the eft auricle with tricuspid regurgitation^

?872 Hat mT ^Med-^ «<flE. April I?
Ib72, Plate III. Fig. 16). b, taken by Dr. Galabin, bv
means of his cardiograph, in a case of mitral regurgitation
in which the left auricle was dilated and hy^eiSphTed
(' Guy's Hospital Reports," 1875, Plate III. Fig. 6).

evidence of a strong auricular systole would be a
feature of the cardiography tracings in this condition
and so would be a valuable aid to diagnosis. That
in some cases of mitral stenosis exaggeration of emi-
nence a, is a feature of the trace, is undoubted. This is

2G6

AURICULAR SYSTOLE.

seen in Fig. 37 A, a, b (see also Dr. Galabin's tracings,
" Guy's Hospital Reports," loc. cit., Plate III. Figs. fJ
and ±5). A reference to the other tracings taken in
cases of* mitral stenosis will at once show, however,
that a strong development of eminence a is by no
means a constant feature; the reasons for this we
shall presently discuss. We may premise that when
in a cardiogram, from a case of mitral stenosis, emi-
nence a is exaggerated and in its normal jjosition, the
auricle is hypertrophied, and there is no extreme
narrowing of the orifice, but the momentum of blood
entering the ventricle is augmented by the abnormal
force of the auricular contraction.

PULSE-TRACE IN MITRAL STENOSIS. 267

VII.

Evidence obtained by the graphic method in valvular
diseases— Mitral Stenosis— Sphygmographic signs— Dif-
ferent views as to irregularity of pulse— Interpolated pul-
sations—Cardiographic evidence— Explanation of interpo-
lated pulsations— Three forms of heart-trace in mitral
stenosis— Tracings showing exaggeration of auricular systole
—Tracings indicating that the auricle adopts an unusual
rhythm— Tracings indicating a causation of the presystolic
murmur independently of the auricle.

We proceed now to consider the chief signs,
afforded by the sphygmograph and cardiograph in
valvular diseases.

I. Mitral Stenosis.— The sphygmographic evi-
dence in cases of mitral stenosis is usually very
characteristic. Various opinions have been expressed
as to the general characters of the pulse in this con-
dition. For the most part observers have attributed
some irregularity to the pulse, but recently Dr.
Hayden has combated this view, contending that in
the earlier stages of the disease « the pulse of mitral
obstruction is usually quite regular, and not abovo
ninety m the minute, but small j" and that marked
irregularity occurs only in the advanced stages of the
disease when the left ventricle begins to fail, and
congestion of the lungs, engorgement of the rio-ht
chambers of the heart, general venous obstruction,
and anasarca have taken place* This experience by
no means agrees with my own, for I have generally

* " Diseases of Heart and Aorta," p. 895.

268 PULSE-TRACE IN MITRAL STENOSIS.'

found that a notable irregularity is the distinguish-
ing1 mark of the sphygmographic tracing in mitral
stenosis, and that this is rendered evident in very
early stages of the disease, even when there may he
no sign of cardiac discomfort whatever. The first
two tracings of Fig. 35 were taken from a case in
which a t}rpical presystolic murmur had become
developed whilst there were no signs pointing to

Fig. 35.

The pulse-trace in three cases of mitral stenosis. The two
first sphygmograms taken by Mahomed's instrument at
different times in a single case ; the two lower taken by
Pond's instrument. All show interpolated pulsations.

cardiac mischief. It will be noted that in the top-
most tracing the second pulsation is followed by a
third before the base-line is reached, and in like
manner the fourth is followed by the fifth. These
interpolated pulsations are also seen with still more
marked pronunciation in the second tracing, and here
it will be noted that after the fourth pulsation there
is a prolonged diastole corresponding to an inter-

PULSE-TRACE IN MITRAL STENOSIS. 260

mission or missed pulsation. After treatment by
digitalis, the pulse was rendered slower, and the evi-
dence of irregularity was only seen in the varying-
intervals between the systoles. Such peculiarity in
the sphygmograms in mitral stenosis has been
thoroughly recognized and described by Dr.
Mahomed.* He mentions that the irregularity may
be made more evident after the influence of digitalis.
I have just asserted the converse, but I have no
doubt that both propositions are true — the rhythm of
the heart is altered by digitalis sometimes in the
sense of developing, sometimes in that of controlling-
the irregularity. Muscular exercise, or any form of
respiratory trouble, will develop or increase the
tendency, and in any doubtful case sphygmograms-
should be taken in the two conditions of tranquillity
and excitement after exercise.

We may conclude, therefore, that a pulse-tracing
which shows irregularity in the diastolic periods
sometimes missed pulsations, and, as described by
JJr. B. foster, the occasional appearance of a small
abortive pulsation in the line of descentf is very
strong evidence of the existence of mitral stenosis.

We may now inquire as to the probable meaning-

t vi r^\Tin?- Jt haS b6en c°™dered by!
J3r. Foster that the rise m the line of descent is due

to a premature auricular contraction which propa-
gates i self - to the ventricle - but this proposition^

consist of all the elements of a ventricular systole. It
always occurs after the dicrotic wave of the tracino

" — ■ . o

* Cf. Medical Times and Gazette Mav is iqto rnn
427, Plate IV. may, 18, 1872, pp. 570 and

t "Clinical Medicine," p. 321.

"270

PULSE-TRACE IN MITRAL STENOSIS.

which precedes it. It is clear, therefore, that it is
an abnormal repetition of a whole cardiac cycle.
The conditions of its occurrence are, according to
Dr. Mahomed, these :—" The left auricle, unable to
thoroughly evacuate its contents, owing- to the
obstruction at the mitral orifice, remains more or less
full, and is generally distended at the termination of
the ventricular systole, during which time it has
been receiving more blood. It is thus stimulated to
contract, and this it does slowly and with effort. But
this is not always the case. The ventricle will not
adapt itself to the altered rhythm of the auricle, but
contracts immediately after the latter ; and when this
occurs earlier than usual, following immediately the
termination of the previous contraction of the ven-
tricle, it gives rise to another peculiarity in rhythm

namely, the secondary contraction of the ventricle."

By this altered correlation between rhythm of auricle
and ventricle may be explained— (1) the occasion-
ally skipped pulsation, the long wait in diastole, and
the irregularity in time of the diastolic period;
(2) the supernumerary systoles. We may have
.slightly to modify this explanation by ascribing to
tension in the passive auricle, as well as contraction
of its muscle, the initiation of irregular ventricular
systole.

CardiograpMc Evidence in Mitral Stenosis. — Inspec-
tion of the cardiac tracing in series shows the same
irregularity that is rendered evident in the tracing of
the pulse. If you turn to Fig. 27, which is a cardiogram
taken in the later stages of mitral stenosis, where the
right heart has consecutively suffered, and there is
tricuspid regurgitation, you will observe that the
characteristic is notable irregularity m time and

HEART-TRACE IN MITRAL STENOSIS. 271

volume. The diastolic periods greatly vary, and the
systoles show differing- degrees of magnitude. Turn
now to the tracings in Fig. 36, where compensation is
much more marked. In a and c there are varying
characters of the diastolic portions, hut d gives the
explanation of the interpolated rise which is seen in
the descending line of the sphygmogram. You will

Pig. S6,

stenoS^Aiy/^r'8 caif°graph in cases of mitral
?™v -n t •°11,ing' °r bu 5.bhnS P^ystolic murmur
at apex, b, Typical presystolic murmur, c, Variable
. presystolic and systolic murmurs, n, Presystol c and
systolic murmurs at apex. e»ysranc ana

notice that in the second pulsation in d, the descend-
ing line -of the cardiac trace fails to reach the base-
line but is succeeded by a second pulsation, after
which the line reaches its usual level ; the same pecu-
liarity is seen in the 5th and 6th pulsations. In
some tracings two pulsations may be observed to

272 HEART-TRACE IN MITRAL STENOSIS.

occur with no horizontal diastolic period separating1
them ; in others only a slight eminence divides them*
It is evident, therefore, that the rise in the down-
stroke of the sphygmogcam is due to a complete
systole of the left ventricle, the condition of the
normal rhythm being so altered, that two systoles
may succeed each other with a very slight or an
inappreciable interval.

We will now examine the characters of the heart-
tracings in mitral stenosis as individual revolutions.
We may divide these into groups.

(1.) Tracings in which the auricular systole is well
marked. I have already said that the only legitimate
deduction from an abnormal development of the emi-
nence a is hypertrophy of the auricle, which may or may
not co-exist with mitral stenosis (see Fig. 34). Fig.
37b shows it considerably increased in a case mani-
festing well-marked presystolic murmur and thrill.
In Fig. 36a, the auricular rise seems not only to be
very pronounced, but to contribute to the general
elevation normally caused by the systole of the ven-
tricle.! In Fig. 37a it is seen that the elevation,
which in all probability corresponds with the auricula-
contraction, has a double summit, and that this may
be an indication of the vibration felt by the hand as
a presystolic thrill. Similar tracings have been
fie-ured by Dr. Galabin. (Note especially Plate III.
Fig. 10, in » Guy's Hospital Eeports," 1875.) In one
case, the period occupied by the heightened, broad-

* Vide Figs. 33, 37c, where some of the systoles are divided
only by a single eminence. . .

t This is also seen, as produced by the high tension in the

auricle, in Fig. 27.

CARDIOGRAMS IN MITRAL STENOSIS. 273

ened, and reduplicated auricular portion of the tracing
could be felt by the finger to be synchronous with
" a slight beat, accompanied by a thrill, just preceding
the main impulse." There can be no room for doubt"
therefore, that an enlarged auricular eminence may be
a feature of the tracing of mitral stenosis ; and further-
Fro. 37.

stenosi g a I Gal'^ Ya^ "graph in ™™ of mitral
stenosis, a a well-marked harsh presystolic murmur
at apex, with thn . B well-marked presystolic m u£n™
and thrill c, well-marked presystolic bruit occ unvfn"
greater portion of diastolic pausefat first of low SB
rolling m character, becoming rasping and vibratorv
and increasing in intensity up to a sudden stop wS the
first sound. D presystolic murmur of low pitch a svs
tohc murmur also at aortic cartilage). 1 ( 3

more, that it is an indication of the auricular-systolic
causation of the murmur and thrill. A very slight
consideration of the conditions would, however su-
gest the probability that in many cases this auricular
r.se would not be manifest. The contraction of the
auricle could not so influence the ventricle as to cause

274 CARDIOGRAMS IN MITRAL STENOSIS.

it to describe an elevation if the entry of blood were
impeded owing- to a very marked degree of stenosis.
Supposing there were no stenosis, and yet marked
hypertrophy of the auricle, we might presuppose a
greater rise in the auricular period than would occur
in the condition of obstruction. Both these proposi-
tions are established by facts. We may conclude that
if in any tracing we see a decided increase of ampli-
tude of the auricular elevation, there is, from some
j cause, auricular hypertrophy ; if there should be the
; physical signs of mitral stenosis, it is most probable
that this hypertrophy is induced by the valvular
! lesion ; if the auricular elevation is not only increased
but broadened, and presenting undulations of its sum-
mit, the probabilities of mitral stenosis, even Avhere
the other physical signs are doubtful, are very con-
siderable. We turn now to another section of cases
of mitral stenosis, in which there are —

(2.) Tracings indicating that the auricle adojrts an
unusual rhythm. That the auricular systole may be
L modified, is proved by the tracings we have just con-
sidered ; the, bifid or interrupted summit of the eleva-
tion, which occupies the position of that known to be
due to the auricle, leaves no room for doubt. I have
■ observed this character in many tracings. Dr. Gala-
bin has shown, however, that the rhythm of the
auricle may be perturbed and altered in far greater
degree. In the tracing (Fig. 38) it will be noticed
that the two diastolic periods which are figured are
abnormally lengthened. In the first of these periods
are two elevations,- a, a; these were found to corre-
spond to two faint pulsations, which were not only
■ audible but visible as slight waves in the fourth inter-
costal space. They were not abortive systoles, for no

CARDIOGRAMS IN MITRAL STENOSIS. 275

sign of them was presented in the pnlse-trace— there
could he no doubt that they were produced by the
contractions of the auricle. In the second diastolic
period it is seen that the elevation indicating the
auricular systole occurs, not in its normal position
just before the systole of the ventricle, but nearly in
the midst of the diastolic portion of the trace. It is
evident, as Da Galabin has said, that " we have here
a heart, the auricle of which sometimes contracted
twice m the interval between two ventricular pulsa-
tions, and sometimes singly in the midst of a lorn-

Fig. 3S.

Heart-tracing, showing urmsual rhythm adopted bv th*
. 7st pfaftfceeriTGa4bi15()':

pause instead of just before the systole of the ven-
tricle. ' In the case from which this cardiogram was
taken, there was no proof from the other physical
signs that mitral stenosis was present. Dr. Galabin
has adduced it as showing that - it is d priori not im-
probable that, in mitral stenosis, the auricle, perturbed
m its action by the obstruction in front, may adopt an
unusual rhythm." Further experience, in m/own
opinion, abundantly confirms this view. If you refer
to Fig. 37 c you will observe that the line indicate
the rise of blood-pressure in the ventricle is broken
into several eminences and depressions, so that it

27G CARDIOGRAMS IN MITRAL STENOSIS.

■would be difficult to say which of these represented
the auricular systole. In d a still stronger illustra-
tion is afforded," the diastolic period being- represented
by an undulatory line containing- four or five emi-
nences or swellings. In Fig. 40 you notice that the
prolonged diastolic period is represented by a sinuous
line more uniform and rounded. In some of the
cardiograms of mitral stenosis figured by Dr. Galabin,
the rise of blood-pressure in the ventricle is marked
by a sudden elevation, followed by a vibratory line
reaching quite up to the next ventricular -systole
{loo. cit., Plate III. Figs. 11 and 13). The sudden
rise can only be explained by the systole of the
auricle, whilst the vibratory line indicates the expul-
sion of the blood from the auricular into the ventricu-
lar cavity. I have met with many tracings in mitral
stenosis which can only be explained on the hypo-
thesis that the auricular systole is exaggerated and
occurs abnormally early. In some such tracings the
line following the rise is broken only by fine vibra-
tions ; in others there are two, three, or four more
pronounced elevations, such as are seen in Fig. 37 d.

In some tracings, however, in cases of mitral steno-
sis, it is impossible to tell where the contraction of the
auricle is recorded, because the whole diastolic period
is marked by a serrated or vibratory line. Good
examples of this are seen in Figs. 33 and 40. It is
also to be observed in Fig. 36, b and d, and m c m
some of the diastolic intervals. It is demonstrated by
many cases that these vibrations may be the graphic
records of thrill or murmur, or both thrill and mur-
mur. They are highly characteristic of the lesion j
and furthermore, in my opinion, they point the lesson
that the presystolic murmur is not always auricular-

CA11DI0GHAMS IN MITRAL STENOSIS. 277

systolic. Sucli view was advanced by Dr. Wilks
("Guy's Hospital Reports," 1871), who, observing- that
some presystolic murmurs extended throughout the
whole period from the second sound to the succeeding-
first sound — that is, through the pause as well as
through the auricular systole— considered that the
first portion of such murmur was due to the blood-
fiow, unaided by the systole of the auricle, through
the narrowed orifice. Experimental proof that such
is possible has been afforded by Marey : if in an arti-
ficial schema of the circulation a perforated plug be

Fig. 39.

Cardiogram (by Pond's instrument) in a case of mitral
stenosis, showing coarse vibrations corresponding to a
presystolic murmur of low pitch and presystolic thrill.

interposed between auricle and ventricle so as to imi-
tate the contracted mitral orifice, a diastolic murmur is
produced when the pressure within the auricle exceeds
a certain point. In such case, therefore, the murmur
starts immediately from the second sound. And this
seems to be only in exact accordance with probabilities
—in the dilatable cavity formed by the auricle and
pulmonary veins the blood, after being impelled by the
Tight ventricle, when exit is impeded by considerable
■contraction of the (mitral) orifice, must be subject to
pressure. The walls of the cavity into which it is
forcibly injected are elastic as well as contractile and

278 : CAJtDIOGItAMS IN MITRAL STENOSIS.

it is only/reasonable to infer tliat the pent-up tension
in the cavity may he a cause of* the early flow into the-
ventricle hetbre such flow is aided hy the proper systole
of the auricle. Dr. Galabin, from cardiography evi-
dence, has formed the opinion that the presystolic-
murmur may in some cases be produced independently
of the auricle, and I am entirely in accord with him.
The positive proof of the proposition is, I consider,,
afforded hy the next section — viz.,

(3) Tracings in which the auricular systole preserves its
normal position. The tracing (Fig. 40) was from a little-

Fig. 43.

Cardiogram from a case of mitral stenosis with presy-
stolic thrill and murmur, showing the auricular systole
in the normal position.

girl, in whom there was apresystolic thrill with localised
presystolic murmur at the apex. The child suffered
from right hemichorea. In the cardiogram the auri-
cular systole is marked in all the individual cycles, and
is in its normal position just before the ventricular
upstroke ; it is obvious that the cause of the thrill
and murmur must have been in this case independent
of the auricular systole.

The cardiography evidence, then, in mitral stenosis-
may be (a) an increase in magnitude of the elevation

CARDIOGRAMS IN MITRAL STENOSIS.

279.

denoting- the auricular systole ; (h) an increase in its
breadth with a summit broken by undulations, a
condition often felt by the finger as a thrill ; (c) a
perturbation of its rhythm so that it may contract at
abnormal periods in the diastolic pause and may repeat
its contractions; (d) a series of vibrations in the line
denoting the rise of blood-pressure within the ventricle,
often expressed also by presystolic murmur and thrill,
find due sometimes to the prolonged auricular systole,
sometimes to the accumulated pressure in the left
auricle unaided by the contraction of the latter, and
sometimes to both cases— viz., tension within the
auricle at the commencement of the period of filling
<«f the ventricle, aided subsecmently by the muscular
effort of the auricle.

280 SPIIYGMOGRAMS IN MITRAL REGURGITATION.

VIII.

Graphic evidence iu valvular diseases continued— Mitral
Regurgitation — Sphygmograms often not characteristic —
Two especial forms — (1) Pulse small, any elevation obtained
with difficulty — Irregularity not observed until right
chambers begin to fail — (2) Pulse ample, but of low tension
— Cardiograms in mitral regurgitation — Ventricular hyper-
trophy distinguished from ddatation by breadth of summit —
Vibrations caused by murmur — Occasional bifurcation of
summit — Shortened diastole — Indication of auricular sys-
tole— Tricuspid Eeguegitation — Arterial pulse-trace
showing curves of respiration — Venous pulse-trace — Traces
from pulsating liver — Characteristics of venous pulse-trace
— The anadicrotic and katadicrotic waves — Cardiograms
indicating irregularity — Right auricular systole not propa-
gated so as to produce elevation in apex-trace, bnt back-
wards, producing anadicrotic wave in veins.

II. Mitral Regurgitation. — The pulse-trace in cases
of mitral regurgitation is often by no means character-
istic. Where compensation is fairly maintained it
may present no features differing from the normal.
The notable forms of the pulse altered by the condition
of mitral regurgitation can, according to my observa-
tions, be divided into two classes. In one of these
divisions the elevation is slight, the upstroke sloping.
It is often difficult, on account of the small calibre of
the artery, to obtain satisfactorily a graphic record ;
the systolic expansion is only represented by a slight
rise, and the details of the gradually sloping down-
stroke are undecipherable. In such instances there
is, owing to the regurgitation, only a very small

SPHYGMOGRAMS IN MITIIAL REGURGITATION. 281

amount of blood thrown into the aorta; but the
arteries are contracted upon their content. The
sloping- upstroke is an indication that the point d'appui
afforded by the mitral valve in its normal state is
impaired ; the current which should produce the ele-
vation flows not only towards the arteries, but back-
wards into the auricle. It is generally supposed that
a great characteristic of the mitral pulse is irregularity.
So far as the mere valvular lesion is concerned, I do
not agree with this view. The peculiar perturbation
of rhythm which I have described in mitral stenosis,
I do not think occurs in uncomplicated regurgitation.
On the other hand, I am perfectly aware that very
marked irregularities of time and volume are often-
times features of the pulse-traces in mitral regurgita-
tion. These characteristics closely resemble those of
the tracing, Fig. 19, which I considered to represent
no valvular lesion. What, then, is their significance ?
I believe that they are complications of the trace
induced by the secondary engorgement of the rir/ht
chambers, by degeneration of the heart-muscle, or 'by
both these causes combined. It is needless to say
that, if this view be correct, it affords an important
guide to prognosis and treatment. If in a case pre-
senting the physical signs of mitral regurgitation you
obtain a tracing showing a sloping upstroke with
irregularity of time and volume, enjoin rest and
endeavour carefully to strengthen the ventricle by
administering iron and digitalis; if; on the other
hand, the tracing nearly approaches the normal, you
may conclude that compensation is good, and anxieties
at the present may be allayed. The action of
digitalis, in conditions of irregularity arising from
mitral regurgitation, is distinctly registered up°on the

282 SPHYGMOGRAMS IN MITRAL REGURGITATION".

pulse-trace. It is remarkable how the disturbances
of ill- compensation may be controlled, and an almost
undecipherable tracing- reduced from chaos to order.

The second of the forms of tracing- in mitral re-
g-urg-itation to which I would call attention differs
greatly from the former. In this case the tracing is
easily obtained, the artery not being small and con-
tracted, and the great feature is the pronounced dicrotic
ivavc. This is well marked in the pulse tracing of
Fig. 41. Here the pulse is fully dicrotic, the artery
being relaxed and the capillary circulation engorged.
In mitral regurgitation the appearance of a strong-

Fig. 41.

Cardiogram and sphygmograin, from a case of free
mitral regurgitation.

dicrotic wave, associated sometimes with a full tidal
wave, is a sign of considerable obstruction in the
capillaries: such traces we meet with in cardiac
dropsy.

We turn now to the cardiac trace in conditions ot
mitral regurgitation. Inspection of the systolic
portion of the trace indicates whether hypertrophy
predominates over dilatation. If the condition be
that of dilatation of the left ventricle, the upstroke
is sudden and lofty, and the descent is also rapid.
If, on the other hand, hypertrophy [predominates,

CARDIOGRAMS IN MITRAL REGURGITATION* 283>

the breadth of the 'systolic eminence is increased.
The truncated summit is sometimes broken by serra-
tions or undulations, indications of which are seem
in Figs. 30 and 36 d. I have no doubt that these
may be the result of the sonorous vibrations of the
systolic murmur, just as we have seen that those
occupying- portions of the period of diastole may-
correspond to the presystolic murmur. There is this-
difference, however, in the record of sound in the
two cases — the vibrations of the presystolic murmur-
are only written in the exact line of the cardiac
trace, whilst it would appear that the vibrations of
a systolic murmur may be communicated to a much
wider area of the chest-wall, so that they may inter-

Fig. 42.

Cardiogram in a case of mitral regurgitation : a, taken
at exact apex ; b, taken in area of loud systolic murmur
showing sonorous vibrations.

mingle, as it were, with the proper elements of the
tracing. This is illustrated by Pig. 42. At a the:
trace is unmodified ; but at b, the position of the lever
being slightly altered, a number of coarse vibrations,
which I consider to be due to a loud systolic murium'
which was manifested in the case, are interposed.
Another character which I have observed in cardiac
tracings, m cases of mitral regurgitation, is the

doubling

forking

of the summit, which

is so-

284 CARDIOGRAMS IN MITRAL REGURGITATION.

marked in Fig-. 42 a. The like is seen in Figs. 32,
30 c, and 41. The explanation I consider to be this :
— After the first ascent of the lever, due to the
hardening and rounding of the ventricle, there is a
fall, because the ventricle has lost the point aVappui
afforded by the stretched curtains of the normal valve ;
the continuing contraction of the ventricle, however,
renews the elevation at the end of the systole.

The diastolic portion of the trace, when there is
any considerable mitral regurgitation, is shortened ;
the ventricle is filled more rapidly than under
normal conditions. In some cases, as in Fig. 41,
the rapid rise of blood-pressure causes a marked
eminence, ending with a fall previously to the systole
of the ventricle. In cases of mitral regurgitation,
in which an increased volume of blood is impelled
by a hypertrophied auricle, the eminence corre-
sponding to the auricular systole is unduly developed
(see Fig. 34).

III. Tricuspid licnnrgitation. — The chief charac-
teristic of the trace of the arterial pulse in tricuspid
regurgitation is undulation of the oasc-linc, marking
the variations of arterial tension during respiration.
If in any case manifesting much dyspnoea, and accom-
panied by engorgement of the right chambers of the
heart, a line drawn through the bases of the upstrokes
shows a series of marked curves, the probability of
tricuspid regurgitation must be taken into account.
So, also, in other valvular diseases, when a pro-
nounced degree of respiratory curve is a superadded
condition, it may be considered probable that the
tricuspid has become insufficient.

In tricuspid regurgitation, however, graphic evidence
.may be obtained from the venous, as well as from the

TRICUSPID REGURGITATION : SPH YGMOGRAMS. 285>

arterial, system. A tracing may be taken of the venous
pulse from the jugular or subclavian. Fig. 43 shows
the graphic characters of such a tracing. The most
conspicuous feature is the pronounced wave which pre-
cedes the main npstroke ; this is due to the systole
of the right auricle, which causes a reflux into the
venous channels. In the descending curve is seen a
sharply-defined notch, analogous to the aortic
(dicrotic) notch of the arterial trace. Tracings may

Fig. 43.

Tracing from subclavian vein in a case of tricuspid

^rgl^/ VVlth miH .CODtl™tion, after Galabin
(Med Uur. Trans., vol. lvm. p. 365, Fig. 3); a, ana-
crotic wave due to systole of auricle; b, katadicrotic
wave analogous to dicrotic wave of arterial pulse.

also be taken over the seat of pulsation of the liver when
m tricuspid regurgitation this is observed (Fig. 45)
In such case the correspondence with the venous° pulse
will be noticed. There is the wave in the principal
upstroke due to the auricular systole, and called the
anadicrotic wave, and that in the downstroke the
katadicrotic wave. The latter seems to be produced
by like causes with those occasioning the dicrotic wave
m the arterial pulse, and maybe the more pronounced
as the veins are dilated and tensionless.

The Cardiac Tkace in tricuspid regurgitation pos-
sesses no special characteristics, but in series it shows.

286 TRICUSPID REGURGITATION : CARDIOGRAMS.

that the systoles are irregular and unequal in volume
(see Fig-. 2?). In the individual tracings the hyper-
trophy of the rif/M auricle is not marked; such
hypertrophy is rather indicated by the venous reflux,
•as shown in the tracings from the pulsating veins
which Ave have just considered. When, therefore,
you observe a very marked auricular eminence in a

Fig. 44.

Tracing from pulsating liver in tricuspid regurgitation,
showing a slight anadicrotic and a pronounced kata-
dicrotic wave.

cardiac tracing, taken in a case of tricuspid regurgi-
tation, you should suspect hypertrophy of the left
auricle. This is strikingly exemplified in a case
recorded by Dr. Mahomed, in which there waj tri-
cuspid regurgitation, with pulsation of the large veins,
in the neck, and in which the apex-tracing showed
the strong auricular elevation, Fig. 34 A. The ne-
cropsy in this case showed a dilated right ventricle
.and wide tricuspid orifice, with greatly hypertrophied
left auricle, but no valvular disease.*

* Med. Times and Gaz., April 13, 1S72, p. 429.

AORTIC REGURGITATION : SPH YGMOGRAMS. 287

IX.

Graphic evidence in valvular diseases, concluded— Aohtic
Regurgitation— Pulse-tracings referred to two types— A
associated with effects of rheumatic endocarditis-High
percussion upstroke— Suddenness— Effacement of dicrotic
wave, and its significance— Flatness of diastolic portion —
' ^^cated with atheronia-Trace of high tension— Heart
tracings- -Evidence of slowness of systole— Signs of hyper
trophy of left ventricle-Shortening of diastole-Ano,
merited blood pressure in the ventricle-Indications of
d>astolic thriU-AoRTic STmosis-Pulse- trace in extreme
cases showing tidal wave only-Evidence when tidal wave
rises above percussion-Estimation of degree of stenosis
when combined with regurgitation-iW.,mce occasionally
registers sonorous vibrations - Vibrations recorded in

STENOSIS OF THE PULMONARY ARTERY.

IV Aortic Regurgitation. The pulse-trace
vvnicn m cases of aortic regurgitation is usually Whir
characteristic, may be referred to one of two types
one of which (A) is usually associated with changes in
the valves due to rheumatic endocarditis, and the other
(13) with the incompetence due to degeneration of the
aorta— aortitis deformans, or senile change
• A'f Tlu PuIf "Jrace P^ents characters correspond-
ing to the splashing, water-hammer pulse of aortic
regurgitation The first point to be noted is, that the
upstroke is loftier than normal. You find that the
spirogram in such cases is easy to take. At low
pressures the tracing shows great amplitude. The
grasp of the strong left ventricle impels a sudden wave
mto arteries, lax at the moment of systole because of

1288 AORTIC REGURGITATION : SPHYGMOGRAMS.

the leakage which has occurred during diastole
through the imperfectly closed aortic aperture.

This suddenness of impulsion gives rise to the lofty
percussion wave recorded by the sphygmograph (vide
TVs. 45 and 46), as it does to the hammer-like quality
ofthe pulse felt by the finger. Next in point of
importance, as characteristic of the sphygmograms of
aortic regurgitation, is impairment or effacement of the
dicrotic wave. This would appear to be a priori pro-
bable. As the dicrotic wave is caused by a rehound

Fig. 45.

Tracing from Brachial. Artery in a case of free aortic regurgi-
tation, showing effacement of dicrotic wave.

from the closed extremity of the aorta, it is only rea-
sonable to infer that, if the closure be imperfect, the
dicrotic wave will also be ill-pronounced. That it
may be so is proved by many tracings {vide Fig. 45).
In the early days of the application of the sphygmo-
o-raph it was considered that this impairment ot the
dicrotic wave was the chief sign of aortic regurgita-
tion : such view is not, however, borne out by tacts.
Aj3 a positive sign, effacement of dicrotism is ot very
high value, for it indicates very free aortic regurgita-

AORTIC REGURGITATION— SPHYGMOGRAMS. 289

tion. It must not be concluded, however, that the
presence of a marked dicrotic wave negatives regurgi-
tation. In Fig. 46 a, you notice that the tracing of
the radial, taken with Pond's instrument, has great
altitude of percussion, the characteristic of aortic
regurgitation : there is a sharply defined tidal wave,
and near the base of the tracing is a weli-marked
dicrotic wave. In this case there was undoubted
aortic regurgitation, and it. is well proved that in such
cases a pronounced dicrotic wave maybe recorded, the
partially-closed aortic cusps forming a sufficient point

Fig. 46.

Tracing from radial artery in aortic regurgitation : a,
taken with light pressure showing dicrotic wave near the
base-line ; b, with slightly increased pressure showing
obliteration of dicrotic wave.

d'appui for its production. It will be noticed, however
that in the tracings in which the percussion upstroke
is high, the dicrotic wave, though it may be amply
developed, is low or near the base-line. Another point
of importance is its easy obliteration by pressure. In
the type of aortic regurgitation, which we are now
considering, I have said the elements of the trace
are best brought out by low pressure, then the dicrotic
wave may be full and rounded; but if the pressure
upon the artery be only slightly increased, the wave
may be altogether obliterated. This characteristic of

290 AORTIC REGURGITATION — SPIi YGMOGHAMS.

the pulse of aortic regurgitation is demonstrated with
great facility l>y Pond's sphygmograph. You com-
mence to take the trace with low pressure, and all the
elements of the trace hecome well marked, as seen in
Fig-. 40 a, which shows the dicrotic wave full and
rounded. Then if, whilst the slide is travelling, you
slightly increase your pressure upon the artery, you
find that the dicrotism is obliterated, as shown in
Pig. 40 b, the diastolic portion of the tracing being'
rendered flat. We may conclude, then, as regards those
sphygmograms of aortic regurgitation which present a;
high elevation that the dicrotic wave is either obvi-
ously impaired or else, though apparently pronounced,
is easily obliterated by increase of pressure* This leads
tis to the third characteristic of such pulse traces, which
is. flatness of the diastolic portion. The line succeeding'
the dicrotic notch is low in the tracing or is horizontal.
Such flatness indicates the emptiness of the artery
during ventricular diastole.

The second type, b, of pulse-trace in aortic regur-
gitation differs considerably from the preceding : there
is no notable exaggeration of the percussion upstroke
■with rapid fall, but a resemblance with the tracings
indicating liir/h tension in the arteries, as in Fig. 24. In
such case the summit of the trace is broadened, the
tidal wave being sustained; the dicrotic notch, though
ill-pronounced, is high in the tracing ; and the gradu-
ally-sloping line corresponding to the diastolic period,
tells of peripheral obstruction. As the former type
of pulse was chiefly associated with the changes in
the aortic valves induced by rheumatic endocarditis,
so this is seen for the most part in conjunction with
degenerative diseases of the aorta and arteries.

So the sphygmograph becomes a valuable means of

AORTIC REGURGITATION — CARDIOGRAMS. 291

diagnosis as regards the two pathological conditions.
For example : a case presents itself with the physical
signs of aortic regurgitation, the patient being past
the prime of life, and giving' a negative or obscure
history of rheumatism. Your sphygmographic tracing
is not of the typical form Fig. 47 a, and you are only
able to conclude from it that there is high tension in the
arteries. Such conclusion is of the highest impor-
tance. It either negatives the conclusion that the
changes are due to rheumatic endocarditis, or indicates
that any regurgitation so produced is slight and well
compensated. But further, in a majority of cases it
goes to prove that the condition giving rise to the
aortic regurgitation is due to atheroma of the aorta —
to endarteritis or aortitis deformans.*

The Cardiac Trace in aortic regurgitation does
not present such important characters in regard to
diagnosis as the pulse trace, but nevertheless affords
evidence of much value. In the first place, it is
noticeable that the quality of suddenness, so marked in
the majority of the sphygmograms, is not a feature of
the cardiograms. In a case in wbich the sphygmo-
graph indicates a lofty, abrupt percussion wave, the
cardiograph demonstrates a slow and prolonged ven-
tricular systole. Dr. Galabin has proved by accurate
measurement, that in a pulse-curve taken in a case of
aortic regurgitation, in which the general shape dif-
fered little from the normal, the upstroke occupied
about one-third less time than that of the healthy
pulse.f On the other hand, " the interval occupied

* Cf. Mahomed, Med. Times and Gaz., Sep. 21 1872 p 3^5
and " Guy's Hospital Reports," 1879, p. 419. '
t Galabin, Med, Chir. Trans., vol. lix. p. 36].

292 AORTIC REGURGITATION — CARDIOGRAMS.

by the main upstroke of the trace, which indicates
the time which the ventricles take in becoming fully
hardened, may be increased in cases of aortic disease
from its normal value of about one-twelfth of a second
to as much as from one-eighth to one-sixth of a second ;
that is to say, that it may be nearly doubled."* The
systolic portion of the tracing- is usually broad, and
the eminence/ well-marked and rounded — indications
of hypertrophy of the left ventricle. In some cases,
however, the opposite condition prevails, the summit
is not truncated but narrow, and the diastolic fall
rapid ; this is an indication that dilatation of the left
ventricle prevails. As regards the diastolic portion
of the tracing, it is very important to note its relative
duration. It is common to find in aortic regurgita-
tion that this is much shortened. There may be
scarcely any interval between one systolic upstroke
and the next, or only a slight single eminence; this
is an indication that the regurgitation is very free, for
the ventricle becomes rapidly filled. Or the diastolic
portion, instead of being horizontal, may present an
ascending line (as in Fig. 31), indicating that the
blood-pressure in the ventricle during diastole be-
comes progressively increased ; this is notably the
case where mitral regurgitation, especially when com-
bined with hypertrophy of the left auricle, co-exists.
Occasionally, vibrations corresponding to diastolic
thrill are marked upon the trace. Such is shown in
certain of the cardiograms recorded by Dr. Galabin
(" Guy's Hospital Reports," 1875, Plate II. Figs. 9
and 10) ; and I have observed it in many others.
In Aortic Obstruction, when the lesion is

* Loc. cit., p. 363.

AORTIC STENOSIS — SPHYGMOGRAMS. 293

extreme, the pulse trace may possess highly distinctive
characters. The percussion wave is effaced, for the
artery, owing- to the narrowing- of the aorta, is slowly
and gradually distended hy the ventricular systole.
The tracing in such cases shows sloping upstrokes
and downstrokes resembling that obtained sometimes
in cases of aneurism (see Fig. 22). Such tracings
are figured by Dr. Mahomed (Medical Times and
Gazette, Aug. 10, 1872, Plate V.) and by Dr. Hayden
("Diseases of Heart and Aorta," p. 869, Fig. LIL).
This last was in the case of a boy aged seven
and a half years. In these cases there is only one
element of the trace, the tidal wave, all else being
obliterated. In other cases the percussion upstroke

Fig. 47.

k K f

X :w i

h 4 00$m

0 Bpyll

Sphygmogram in case of aortic obstruction (Dr. Gala-
lain). A large tidal wave, c d, rises'high above the percussion
•wave, a b, indicating prolonged ventricular contraction;
there is a marked dicrotic wave, e /, indicating that there
is little or no reflux through the aortic orifice ; pulse very
slow.

is arrested, and from its point of arrest proceeds an.
ample tidal wave, which rises high above the per-
cussion wave.* This is seen in Fig. 47. There is
not such extreme narrowing of -the aortic orifice that
the element of suddenness is lost, but the percussion'

* Cf. Galabin, Med. Chir. Trans., vol. lix. p. 384.

294

AORTIC STENOSIS — CARDIOGRAMS.

is short, and the pronounced tidal wave is an indica-
tion of the prolonged systole of the ventricle. So
important do I consider this form of tracing, that I
would say, whenever you meet with a radial
tracing in which the percussion wave is suddenly
arrested and an ample tidal wave rises ahove it,
suspect aortic stenosis.* I have hefore said that the
signs of this lesion are often obscure, and that during
life it often remains undiscovered. As an aid to the
diagnosis of the condition, I think the sphygmograph
is of great value. So also in combined aortic regurgi-
tation and obstruction, a conjunction which is much
more common than either affection singly, you may
take the amplitude of the tidal wave as a measure of
the degree of stenosis. A pulse trace, which at very
light pressure has the typical verticality of aortic
regurgitation with very slight pronunciation of the
tidal wave, may, by increase of pressure, be made
more and more to develop the tidal, and this I con-
sider to be an indication of the accompanying stenosis.
In certain cases of aortic stenosis there is a marked
division between the percussion and tidal waves, so
that the summit of the trace is forked {vide Fig. 47).
Such tracings are figured by Dr. Mahomed (Medical
Times and Gazette, Aug. 10, 1872 ; Plate V. Figs. 47,
48, and 49) ; they may explain the thrill which is
sometimes felt in the pulse of aortic stenosis.

Cardiography Tracings in aortic stenosis are
not often characteristic. Traces taken by Pond's
instrument with very light pressure, over the site of
an aortic systolic murmur, may present vibrations
caused by the conditions which produce the sound.

* Vide Fig. 24, the last tracing.

STENOSIS OF PULMONARY ARTERY.

295.

This is strongly insisted upon by Dr. Pond as a point
of value, but considerable caution must be used in so
accepting- it. These fine vibrations may have many
causes — tremulous movements of the skin, vibrator3r
•contractions of the intercostal muscles, and rhonchi, for
example. Nevertheless, I have had experience that
such vibrations maybe recorded in the area of a systolic
aortic murmur, just as I have already shown them to
be made manifest in mitral regurgitation (see Fig. 42)
and in mitral stenosis (Figs. 33, 36, 37, and 39).
In Stenosis of the Pulmonary Artery also

Fig. 48.

Cardiogram from a case of congenital Cyanosis with
murmur oyer the site of the pulmonary artery: a,
showing vibrations over the maximum of a loud super-
ficial systolic murmur; b. tracing at the apex of the
heart.

such vibrations, due to a systolic murmur, may be
registered upon the trace, as in the example Fig. 48.

INDEX.

Note. — The figures in darker type (e.g., 123) refer to Part II.

PAGE

Abnormal sounds 123

Accent 98

Albuminuria 19

Anadicrotic wave 285

Anaemia - 29,132,156,159, 1 69

Aneurism, pulse-trace in 247

Aortic area 9T

„ obstruction 135,293

regurgitation 43, 50, 73, 144, 212, 287

„ double murmur 147

Aortitis deformans 139, 29L

Apex-beat 44, 56-

„ displacement of 57

Aphonia -18

Apoplexy 16

Aieus senilis 32

Arterial tension 248

Atheroma 48,139,182,291

Auricles, functions of 61

,, pulsations of 64

Auricle, right, hypertrophy of 64, 88, 286

„ left „ 64,186,265,272

Auricular systole 265

Auriculo-systolic murmur 192

Auscultation 90

Basedow's disease 30

Blueness 23

Cardiac cycle 61,258

Cardiograph 228

Cardiography indications 252

Cerebral symptoms 15-

Charts, use of 82

Cheyne-Stokes dyspncea 35

Chorea 15, 17a

CllRONOMETRY OF MURMURS 193-

„ Pulsations 6&

INDEX.

2,97

PJlGK

'Clubbing of finger-ends .

Coma

Combined Murmurs . .
Conduction of murmurs .
Congenital lesions . . .
Convection of murmurs .

Cyanosis

Diastolic murmur . . .

period ....

„ thrill ....
Dicrotic wave ....
Dicrotism . . .
Dilatation

„ apex beat in .

,, dulness in . .
of left ventricle

Dulness, prtecordial 78

Dyspnoea 14, 33

Effort, effect of 55

Embolism . . . . 17, 204

Endocarditis, rheumatic 138, 180, 186

ulcerative 142, 182

villous 135, 141, 182

Etiology 21

Exophthalmos . . 30

Fatty degeneration 105

Foramen ovale, patency of 24, 162

Friction-fremitus : . 71

Friction-sound 124

,, ,, pleuro-pericardial 130

•Goitre, exophthalmic 30

Gouty kidney 20

Graphic records 83

Graphic Representation of Murmurs .197

Graves' disease 30

Haemophilia 250

Haemoptysis 204

Haemorrhage .13

,, intra-cramal 16

Heart-trace, normal 239

„ „ abnormal 254

Hepatic pulsation 69, 285

Hoarseness 18

Hyper-dicrotism 259

Hypertrophy .20, 45, 58, 86, 91, 99, 103

, „ pulse in . 50

„ of right ventricle, pulse in 52

... . . 215
.... 152
.... 161
.... 153
. 14, 24, 162
.... 143
. . . 260
.... 73
. . . 248
. . . 250
. 45, 58, 60
.... 45
.... 87
105, 184, 25 6
.... 39

298

INDEX.

PAGE-

Hypertrophy of right ventricle 60, 87

„ of left ventricle .... 60,87,100,104,256

„ of left auricle 64,186,265,272

'„ concentric 187

Inspection 25

Intermission 12, 53, 241

Intermittent pulse 55

Inter-ventricular septum, opening in 24

Inversion of cardiac trace .• 253

Irregularity . . 12, 53, 253

„ arhythmic . 243

Irregular pulse . . . . .• 53,241, 242,268

Jaundice 31

Katadicrotic wave ...285

Kidney symptoms . . . 19, 29>

Liver, pulsation of . . 69, 285

Locomotive pulse . 43,289

Lung symptoms 14

Mitral area 97

,, ,, murmurs in , 191

„ regurgitation ... 51, 101, 183, 201, 203, 208, 280
„ stenosis ... 65, 108, 185, 200, 203, 209, 267, 270

Murmurs, adynamic 175, 178

„ anamiic 132, 156, 159, 169

,, cause of 147

„ combined 215

„ conduction of 152

„ convection of 153-

,, double aortic 147

„ double mitral 206

„ temporary 132, 170

,, vascular. . . . ... , 155

Myocarditis 174

Normal Heart Sounds . 98

Obstruction, mitral ... 65, 108, 185, 200, 209, 267, 270
„ aortic . . ....... . . .72,135,142,293

pulmonary 26, 160, 163, 295

(Edema 14, 39

Ophthalmoscopy . . .• 144

Orthopnea 33

Pain 3

Pallor . ... . . ■ 29

Palpation 48

Palpitation- . .. .. ..... 11, 254

Percussion 77

Percussion' wave, modifications of 246

Pericardial adhesions 47, 6S

■ .-. • effusion ..... 82

INDEX.

299

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Full text of "Manual of the physical diagnosis of the diseases of the heart [electronic resource] : including the use of the sphygmograph and cardiograph"

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